Current Understanding of the Role of the Brd4 Protein in the Papillomavirus Lifecycle
Identifieur interne : 000151 ( Pmc/Corpus ); précédent : 000150Current Understanding of the Role of the Brd4 Protein in the Papillomavirus Lifecycle
Auteurs : Alison A. Mcbride ; Moon Kyoo JangSource :
- Viruses [ 1999-4915 ] ; 2013.
Abstract
The Brd4 protein is an epigenetic reader that is central to regulation of cellular transcription and mitotic bookmarking. The transcription and replication proteins of many viruses interact with Brd4. We describe the multiple roles of Brd4 in the papillomavirus lifecycle.
Url:
DOI: 10.3390/v5061374
PubMed: 23722886
PubMed Central: 3717712
Links to Exploration step
PMC:3717712Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Current Understanding of the Role of the Brd4 Protein in the Papillomavirus Lifecycle</title><author><name sortKey="Mcbride, Alison A" sort="Mcbride, Alison A" uniqKey="Mcbride A" first="Alison A." last="Mcbride">Alison A. Mcbride</name></author><author><name sortKey="Jang, Moon Kyoo" sort="Jang, Moon Kyoo" uniqKey="Jang M" first="Moon Kyoo" last="Jang">Moon Kyoo Jang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23722886</idno><idno type="pmc">3717712</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717712</idno><idno type="RBID">PMC:3717712</idno><idno type="doi">10.3390/v5061374</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000151</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000151</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Current Understanding of the Role of the Brd4 Protein in the Papillomavirus Lifecycle</title><author><name sortKey="Mcbride, Alison A" sort="Mcbride, Alison A" uniqKey="Mcbride A" first="Alison A." last="Mcbride">Alison A. Mcbride</name></author><author><name sortKey="Jang, Moon Kyoo" sort="Jang, Moon Kyoo" uniqKey="Jang M" first="Moon Kyoo" last="Jang">Moon Kyoo Jang</name></author></analytic><series><title level="j">Viruses</title><idno type="eISSN">1999-4915</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The Brd4 protein is an epigenetic reader that is central to regulation of cellular transcription and mitotic bookmarking. The transcription and replication proteins of many viruses interact with Brd4. We describe the multiple roles of Brd4 in the papillomavirus lifecycle. </p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bouvard, V" uniqKey="Bouvard V">V. Bouvard</name></author><author><name sortKey="Baan, R" uniqKey="Baan R">R. Baan</name></author><author><name sortKey="Straif, K" uniqKey="Straif K">K. Straif</name></author><author><name sortKey="Grosse, Y" uniqKey="Grosse Y">Y. Grosse</name></author><author><name sortKey="Secretan, B" uniqKey="Secretan B">B. Secretan</name></author><author><name sortKey="El, G F" uniqKey="El G">G.F. El</name></author><author><name sortKey="Benbrahim Tallaa, L" uniqKey="Benbrahim Tallaa L">L. Benbrahim-Tallaa</name></author><author><name sortKey="Guha, N" uniqKey="Guha N">N. Guha</name></author><author><name sortKey="Freeman, C" uniqKey="Freeman C">C. Freeman</name></author><author><name sortKey="Galichet, L" uniqKey="Galichet L">L. Galichet</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Walboomers, J M" uniqKey="Walboomers J">J.M. Walboomers</name></author><author><name sortKey="Jacobs, M V" uniqKey="Jacobs M">M.V. Jacobs</name></author><author><name sortKey="Manos, M M" uniqKey="Manos M">M.M. Manos</name></author><author><name sortKey="Bosch, F X" uniqKey="Bosch F">F.X. Bosch</name></author><author><name sortKey="Kummer, J A" uniqKey="Kummer J">J.A. Kummer</name></author><author><name sortKey="Shah, K V" uniqKey="Shah K">K.V. Shah</name></author><author><name sortKey="Snijders, P J" uniqKey="Snijders P">P.J. Snijders</name></author><author><name sortKey="Peto, J" uniqKey="Peto J">J. Peto</name></author><author><name sortKey="Meijer, C J" uniqKey="Meijer C">C.J. Meijer</name></author><author><name sortKey="Mu Oz, N" uniqKey="Mu Oz N">N. Muñoz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gillison, M L" uniqKey="Gillison M">M.L. Gillison</name></author><author><name sortKey="Lowy, D R" uniqKey="Lowy D">D.R. Lowy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Johansson, C" uniqKey="Johansson C">C. Johansson</name></author><author><name sortKey="Schwartz, S" uniqKey="Schwartz S">S. Schwartz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Spalholz, B A" uniqKey="Spalholz B">B.A. Spalholz</name></author><author><name sortKey="Yang, Y C" uniqKey="Yang Y">Y.C. Yang</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author><author><name sortKey="Byrne, J C" uniqKey="Byrne J">J.C. Byrne</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Androphy, E J" uniqKey="Androphy E">E.J. Androphy</name></author><author><name sortKey="Lowy, D R" uniqKey="Lowy D">D.R. Lowy</name></author><author><name sortKey="Schiller, J T" uniqKey="Schiller J">J.T. Schiller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cripe, T P" uniqKey="Cripe T">T.P. Cripe</name></author><author><name sortKey="Haugen, T H" uniqKey="Haugen T">T.H. Haugen</name></author><author><name sortKey="Turk, J P" uniqKey="Turk J">J.P. Turk</name></author><author><name sortKey="Tabatabai, F" uniqKey="Tabatabai F">F. Tabatabai</name></author><author><name sortKey="Schmid, P G" uniqKey="Schmid P">P.G. Schmid</name></author><author><name sortKey="Durst, M" uniqKey="Durst M">M. Dürst</name></author><author><name sortKey="Gissmann, L" uniqKey="Gissmann L">L. Gissmann</name></author><author><name sortKey="Roman, A" uniqKey="Roman A">A. Roman</name></author><author><name sortKey="Turek, L P" uniqKey="Turek L">L.P. Turek</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chin, M T" uniqKey="Chin M">M.T. Chin</name></author><author><name sortKey="Hirochika, R" uniqKey="Hirochika R">R. Hirochika</name></author><author><name sortKey="Hirochika, H" uniqKey="Hirochika H">H. Hirochika</name></author><author><name sortKey="Broker, T R" uniqKey="Broker T">T.R. Broker</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Steger, G" uniqKey="Steger G">G. Steger</name></author><author><name sortKey="Corbach, S" uniqKey="Corbach S">S. Corbach</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author><author><name sortKey="Yaniv, M" uniqKey="Yaniv M">M. Yaniv</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bernard, B A" uniqKey="Bernard B">B.A. Bernard</name></author><author><name sortKey="Bailly, C" uniqKey="Bailly C">C. Bailly</name></author><author><name sortKey="Lenoir, M C" uniqKey="Lenoir M">M.C. Lenoir</name></author><author><name sortKey="Darmon, M" uniqKey="Darmon M">M. Darmon</name></author><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author><author><name sortKey="Yaniv, M" uniqKey="Yaniv M">M. Yaniv</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Romanczuk, H" uniqKey="Romanczuk H">H. Romanczuk</name></author><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tan, S H" uniqKey="Tan S">S.H. Tan</name></author><author><name sortKey="Gloss, B" uniqKey="Gloss B">B. Gloss</name></author><author><name sortKey="Bernard, H U" uniqKey="Bernard H">H.U. Bernard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dong, G" uniqKey="Dong G">G. Dong</name></author><author><name sortKey="Broker, T R" uniqKey="Broker T">T.R. Broker</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tan, S H" uniqKey="Tan S">S.H. Tan</name></author><author><name sortKey="Leong, L E" uniqKey="Leong L">L.E. Leong</name></author><author><name sortKey="Walker, P A" uniqKey="Walker P">P.A. Walker</name></author><author><name sortKey="Bernard, H U" uniqKey="Bernard H">H.U. Bernard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nishimura, A" uniqKey="Nishimura A">A. Nishimura</name></author><author><name sortKey="Ono, T" uniqKey="Ono T">T. Ono</name></author><author><name sortKey="Ishimoto, A" uniqKey="Ishimoto A">A. Ishimoto</name></author><author><name sortKey="Dowhanick, J J" uniqKey="Dowhanick J">J.J. Dowhanick</name></author><author><name sortKey="Frizzell, M A" uniqKey="Frizzell M">M.A. Frizzell</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author><author><name sortKey="Sakai, H" uniqKey="Sakai H">H. Sakai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Smith, J A" uniqKey="Smith J">J.A. Smith</name></author><author><name sortKey="White, E A" uniqKey="White E">E.A. White</name></author><author><name sortKey="Sowa, M E" uniqKey="Sowa M">M.E. Sowa</name></author><author><name sortKey="Powell, M L" uniqKey="Powell M">M.L. Powell</name></author><author><name sortKey="Ottinger, M" uniqKey="Ottinger M">M. Ottinger</name></author><author><name sortKey="Harper, J W" uniqKey="Harper J">J.W. Harper</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schweiger, M R" uniqKey="Schweiger M">M.R. Schweiger</name></author><author><name sortKey="Ottinger, M" uniqKey="Ottinger M">M. Ottinger</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, S Y" uniqKey="Wu S">S.Y. Wu</name></author><author><name sortKey="Lee, A Y" uniqKey="Lee A">A.Y. Lee</name></author><author><name sortKey="Hou, S Y" uniqKey="Hou S">S.Y. Hou</name></author><author><name sortKey="Kemper, J K" uniqKey="Kemper J">J.K. Kemper</name></author><author><name sortKey="Erdjument Bromage, H" uniqKey="Erdjument Bromage H">H. Erdjument-Bromage</name></author><author><name sortKey="Tempst, P" uniqKey="Tempst P">P. Tempst</name></author><author><name sortKey="Chiang, C M" uniqKey="Chiang C">C.M. Chiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hwang, E S" uniqKey="Hwang E">E.S. Hwang</name></author><author><name sortKey="Riese, D J D" uniqKey="Riese D">D.J.D. Riese</name></author><author><name sortKey="Settleman, J" uniqKey="Settleman J">J. Settleman</name></author><author><name sortKey="Nilson, L A" uniqKey="Nilson L">L.A. Nilson</name></author><author><name sortKey="Honig, J" uniqKey="Honig J">J. Honig</name></author><author><name sortKey="Flynn, S" uniqKey="Flynn S">S. Flynn</name></author><author><name sortKey="Dimaio, D" uniqKey="Dimaio D">D. DiMaio</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dowhanick, J J" uniqKey="Dowhanick J">J.J. Dowhanick</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Desaintes, C" uniqKey="Desaintes C">C. Desaintes</name></author><author><name sortKey="Demeret, C" uniqKey="Demeret C">C. Demeret</name></author><author><name sortKey="Goyat, S" uniqKey="Goyat S">S. Goyat</name></author><author><name sortKey="Yaniv, M" uniqKey="Yaniv M">M. Yaniv</name></author><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stubenrauch, F" uniqKey="Stubenrauch F">F. Stubenrauch</name></author><author><name sortKey="Zobel, T" uniqKey="Zobel T">T. Zobel</name></author><author><name sortKey="Iftner, T" uniqKey="Iftner T">T. Iftner</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chiang, C M" uniqKey="Chiang C">C.M. Chiang</name></author><author><name sortKey="Broker, T R" uniqKey="Broker T">T.R. Broker</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Powell, M L" uniqKey="Powell M">M.L. Powell</name></author><author><name sortKey="Smith, J A" uniqKey="Smith J">J.A. Smith</name></author><author><name sortKey="Sowa, M E" uniqKey="Sowa M">M.E. Sowa</name></author><author><name sortKey="Harper, J W" uniqKey="Harper J">J.W. Harper</name></author><author><name sortKey="Iftner, T" uniqKey="Iftner T">T. Iftner</name></author><author><name sortKey="Stubenrauch, F" uniqKey="Stubenrauch F">F. Stubenrauch</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pett, M" uniqKey="Pett M">M. Pett</name></author><author><name sortKey="Coleman, N" uniqKey="Coleman N">N. Coleman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Francis, D A" uniqKey="Francis D">D.A. Francis</name></author><author><name sortKey="Schmid, S I" uniqKey="Schmid S">S.I. Schmid</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jeon, S" uniqKey="Jeon S">S. Jeon</name></author><author><name sortKey="Allen Hoffmann, B L" uniqKey="Allen Hoffmann B">B.L. Allen-Hoffmann</name></author><author><name sortKey="Lambert, P F" uniqKey="Lambert P">P.F. Lambert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mohr, I J" uniqKey="Mohr I">I.J. Mohr</name></author><author><name sortKey="Clark, R" uniqKey="Clark R">R. Clark</name></author><author><name sortKey="Sun, S" uniqKey="Sun S">S. Sun</name></author><author><name sortKey="Androphy, E J" uniqKey="Androphy E">E.J. Androphy</name></author><author><name sortKey="Macpherson, P" uniqKey="Macpherson P">P. MacPherson</name></author><author><name sortKey="Botchan, M R" uniqKey="Botchan M">M.R. Botchan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author><author><name sortKey="Stenlund, A" uniqKey="Stenlund A">A. Stenlund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author><author><name sortKey="Ustav, E" uniqKey="Ustav E">E. Ustav</name></author><author><name sortKey="Szymanski, P" uniqKey="Szymanski P">P. Szymanski</name></author><author><name sortKey="Stenlund, A" uniqKey="Stenlund A">A. Stenlund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sanders, C M" uniqKey="Sanders C">C.M. Sanders</name></author><author><name sortKey="Stenlund, A" uniqKey="Stenlund A">A. Stenlund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Piirsoo, M" uniqKey="Piirsoo M">M. Piirsoo</name></author><author><name sortKey="Ustav, E" uniqKey="Ustav E">E. Ustav</name></author><author><name sortKey="Mandel, T" uniqKey="Mandel T">T. Mandel</name></author><author><name sortKey="Stenlund, A" uniqKey="Stenlund A">A. Stenlund</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Skiadopoulos, M H" uniqKey="Skiadopoulos M">M.H. Skiadopoulos</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ilves, I" uniqKey="Ilves I">I. Ilves</name></author><author><name sortKey="Kivi, S" uniqKey="Kivi S">S. Kivi</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bastien, N" uniqKey="Bastien N">N. Bastien</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, K" uniqKey="Kim K">K. Kim</name></author><author><name sortKey="Lambert, P F" uniqKey="Lambert P">P.F. Lambert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Egawa, N" uniqKey="Egawa N">N. Egawa</name></author><author><name sortKey="Nakahara, T" uniqKey="Nakahara T">T. Nakahara</name></author><author><name sortKey="Ohno, S" uniqKey="Ohno S">S. Ohno</name></author><author><name sortKey="Narisawa Saito, M" uniqKey="Narisawa Saito M">M. Narisawa-Saito</name></author><author><name sortKey="Yugawa, T" uniqKey="Yugawa T">T. Yugawa</name></author><author><name sortKey="Fujita, M" uniqKey="Fujita M">M. Fujita</name></author><author><name sortKey="Yamato, K" uniqKey="Yamato K">K. Yamato</name></author><author><name sortKey="Natori, Y" uniqKey="Natori Y">Y. Natori</name></author><author><name sortKey="Kiyono, T" uniqKey="Kiyono T">T. Kiyono</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xue, Y" uniqKey="Xue Y">Y. Xue</name></author><author><name sortKey="Bellanger, S" uniqKey="Bellanger S">S. Bellanger</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W. Zhang</name></author><author><name sortKey="Lim, D" uniqKey="Lim D">D. Lim</name></author><author><name sortKey="Low, J" uniqKey="Low J">J. Low</name></author><author><name sortKey="Lunny, D" uniqKey="Lunny D">D. Lunny</name></author><author><name sortKey="Thierry, F" uniqKey="Thierry F">F. Thierry</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Penrose, K J" uniqKey="Penrose K">K.J. Penrose</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Flores, E R" uniqKey="Flores E">E.R. Flores</name></author><author><name sortKey="Lambert, P F" uniqKey="Lambert P">P.F. Lambert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sakakibara, N" uniqKey="Sakakibara N">N. Sakakibara</name></author><author><name sortKey="Chen, D" uniqKey="Chen D">D. Chen</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gillespie, K A" uniqKey="Gillespie K">K.A. Gillespie</name></author><author><name sortKey="Mehta, K P" uniqKey="Mehta K">K.P. Mehta</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author><author><name sortKey="Moody, C A" uniqKey="Moody C">C.A. Moody</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moody, C A" uniqKey="Moody C">C.A. Moody</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fradet Turcotte, A" uniqKey="Fradet Turcotte A">A. Fradet-Turcotte</name></author><author><name sortKey="Bergeron Labrecque, F" uniqKey="Bergeron Labrecque F">F. Bergeron-Labrecque</name></author><author><name sortKey="Moody, C A" uniqKey="Moody C">C.A. Moody</name></author><author><name sortKey="Lehoux, M" uniqKey="Lehoux M">M. Lehoux</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author><author><name sortKey="Archambault, J" uniqKey="Archambault J">J. Archambault</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sakakibara, N" uniqKey="Sakakibara N">N. Sakakibara</name></author><author><name sortKey="Mitra, R" uniqKey="Mitra R">R. Mitra</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reinson, T" uniqKey="Reinson T">T. Reinson</name></author><author><name sortKey="Toots, M" uniqKey="Toots M">M. Toots</name></author><author><name sortKey="Kadaja, M" uniqKey="Kadaja M">M. Kadaja</name></author><author><name sortKey="Pipitch, R" uniqKey="Pipitch R">R. Pipitch</name></author><author><name sortKey="Allik, M" uniqKey="Allik M">M. Allik</name></author><author><name sortKey="Ustav, E" uniqKey="Ustav E">E. Ustav</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Swindle, C S" uniqKey="Swindle C">C.S. Swindle</name></author><author><name sortKey="Zou, N" uniqKey="Zou N">N. Zou</name></author><author><name sortKey="Van Tine, B A" uniqKey="Van Tine B">B.A. Van Tine</name></author><author><name sortKey="Shaw, G M" uniqKey="Shaw G">G.M. Shaw</name></author><author><name sortKey="Engler, J A" uniqKey="Engler J">J.A. Engler</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Van Doorslaer, K" uniqKey="Van Doorslaer K">K. Van Doorslaer</name></author><author><name sortKey="Tan, Q" uniqKey="Tan Q">Q. Tan</name></author><author><name sortKey="Xirasagar, S" uniqKey="Xirasagar S">S. Xirasagar</name></author><author><name sortKey="Bandaru, S" uniqKey="Bandaru S">S. Bandaru</name></author><author><name sortKey="Gopalan, V" uniqKey="Gopalan V">V. Gopalan</name></author><author><name sortKey="Mohamoud, Y" uniqKey="Mohamoud Y">Y. Mohamoud</name></author><author><name sortKey="Huyen, Y" uniqKey="Huyen Y">Y. Huyen</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, R" uniqKey="Li R">R. Li</name></author><author><name sortKey="Knight, J" uniqKey="Knight J">J. Knight</name></author><author><name sortKey="Bream, G" uniqKey="Bream G">G. Bream</name></author><author><name sortKey="Stenlund, A" uniqKey="Stenlund A">A. Stenlund</name></author><author><name sortKey="Botchan, M" uniqKey="Botchan M">M. Botchan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stubenrauch, F" uniqKey="Stubenrauch F">F. Stubenrauch</name></author><author><name sortKey="Lim, H B" uniqKey="Lim H">H.B. Lim</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Van Doorslaer, K" uniqKey="Van Doorslaer K">K. Van Doorslaer</name></author><author><name sortKey="Khan, J" uniqKey="Khan J">J. Khan</name></author><author><name sortKey="Chapman, S" uniqKey="Chapman S">S. Chapman</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dey, A" uniqKey="Dey A">A. Dey</name></author><author><name sortKey="Ellenberg, J" uniqKey="Ellenberg J">J. Ellenberg</name></author><author><name sortKey="Farina, A" uniqKey="Farina A">A. Farina</name></author><author><name sortKey="Coleman, A E" uniqKey="Coleman A">A.E. Coleman</name></author><author><name sortKey="Maruyama, T" uniqKey="Maruyama T">T. Maruyama</name></author><author><name sortKey="Sciortino, S" uniqKey="Sciortino S">S. Sciortino</name></author><author><name sortKey="Lippincott Schwartz, J" uniqKey="Lippincott Schwartz J">J. Lippincott-Schwartz</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Florence, B" uniqKey="Florence B">B. Florence</name></author><author><name sortKey="Faller, D V" uniqKey="Faller D">D.V. Faller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Houzelstein, D" uniqKey="Houzelstein D">D. Houzelstein</name></author><author><name sortKey="Bullock, S L" uniqKey="Bullock S">S.L. Bullock</name></author><author><name sortKey="Lynch, D E" uniqKey="Lynch D">D.E. Lynch</name></author><author><name sortKey="Grigorieva, E F" uniqKey="Grigorieva E">E.F. Grigorieva</name></author><author><name sortKey="Wilson, V A" uniqKey="Wilson V">V.A. Wilson</name></author><author><name sortKey="Beddington, R S" uniqKey="Beddington R">R.S. Beddington</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dey, A" uniqKey="Dey A">A. Dey</name></author><author><name sortKey="Chitsaz, F" uniqKey="Chitsaz F">F. Chitsaz</name></author><author><name sortKey="Abbasi, A" uniqKey="Abbasi A">A. Abbasi</name></author><author><name sortKey="Misteli, T" uniqKey="Misteli T">T. Misteli</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dey, A" uniqKey="Dey A">A. Dey</name></author><author><name sortKey="Nishiyama, A" uniqKey="Nishiyama A">A. Nishiyama</name></author><author><name sortKey="Karpova, T" uniqKey="Karpova T">T. Karpova</name></author><author><name sortKey="Mcnally, J" uniqKey="Mcnally J">J. McNally</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mochizuki, K" uniqKey="Mochizuki K">K. Mochizuki</name></author><author><name sortKey="Nishiyama, A" uniqKey="Nishiyama A">A. Nishiyama</name></author><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Dey, A" uniqKey="Dey A">A. Dey</name></author><author><name sortKey="Ghosh, A" uniqKey="Ghosh A">A. Ghosh</name></author><author><name sortKey="Tamura, T" uniqKey="Tamura T">T. Tamura</name></author><author><name sortKey="Natsume, H" uniqKey="Natsume H">H. Natsume</name></author><author><name sortKey="Yao, H J" uniqKey="Yao H">H.J. Yao</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, R" uniqKey="Zhao R">R. Zhao</name></author><author><name sortKey="Nakamura, T" uniqKey="Nakamura T">T. Nakamura</name></author><author><name sortKey="Fu, Y" uniqKey="Fu Y">Y. Fu</name></author><author><name sortKey="Lazar, Z" uniqKey="Lazar Z">Z. Lazar</name></author><author><name sortKey="Spector, D L" uniqKey="Spector D">D.L. Spector</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Mochizuki, K" uniqKey="Mochizuki K">K. Mochizuki</name></author><author><name sortKey="Zhou, M" uniqKey="Zhou M">M. Zhou</name></author><author><name sortKey="Jeong, H S" uniqKey="Jeong H">H.S. Jeong</name></author><author><name sortKey="Brady, J N" uniqKey="Brady J">J.N. Brady</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Z" uniqKey="Yang Z">Z. Yang</name></author><author><name sortKey="Yik, J H" uniqKey="Yik J">J.H. Yik</name></author><author><name sortKey="Chen, R" uniqKey="Chen R">R. Chen</name></author><author><name sortKey="He, N" uniqKey="He N">N. He</name></author><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Zhou, Q" uniqKey="Zhou Q">Q. Zhou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Devaiah, B N" uniqKey="Devaiah B">B.N. Devaiah</name></author><author><name sortKey="Singer, D S" uniqKey="Singer D">D.S. Singer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Filippakopoulos, P" uniqKey="Filippakopoulos P">P. Filippakopoulos</name></author><author><name sortKey="Picaud, S" uniqKey="Picaud S">S. Picaud</name></author><author><name sortKey="Mangos, M" uniqKey="Mangos M">M. Mangos</name></author><author><name sortKey="Keates, T" uniqKey="Keates T">T. Keates</name></author><author><name sortKey="Lambert, J P" uniqKey="Lambert J">J.P. Lambert</name></author><author><name sortKey="Barsyte Lovejoy, D" uniqKey="Barsyte Lovejoy D">D. Barsyte-Lovejoy</name></author><author><name sortKey="Felletar, I" uniqKey="Felletar I">I. Felletar</name></author><author><name sortKey="Volkmer, R" uniqKey="Volkmer R">R. Volkmer</name></author><author><name sortKey="Muller, S" uniqKey="Muller S">S. Muller</name></author><author><name sortKey="Pawson, T" uniqKey="Pawson T">T. Pawson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vollmuth, F" uniqKey="Vollmuth F">F. Vollmuth</name></author><author><name sortKey="Blankenfeldt, W" uniqKey="Blankenfeldt W">W. Blankenfeldt</name></author><author><name sortKey="Geyer, M" uniqKey="Geyer M">M. Geyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schroder, S" uniqKey="Schroder S">S. Schröder</name></author><author><name sortKey="Cho, S" uniqKey="Cho S">S. Cho</name></author><author><name sortKey="Zeng, L" uniqKey="Zeng L">L. Zeng</name></author><author><name sortKey="Zhang, Q" uniqKey="Zhang Q">Q. Zhang</name></author><author><name sortKey="Kaehlcke, K" uniqKey="Kaehlcke K">K. Kaehlcke</name></author><author><name sortKey="Mak, L" uniqKey="Mak L">L. Mak</name></author><author><name sortKey="Lau, J" uniqKey="Lau J">J. Lau</name></author><author><name sortKey="Bisgrove, D" uniqKey="Bisgrove D">D. Bisgrove</name></author><author><name sortKey="Schnolzer, M" uniqKey="Schnolzer M">M. Schnölzer</name></author><author><name sortKey="Verdin, E" uniqKey="Verdin E">E. Verdin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, B" uniqKey="Huang B">B. Huang</name></author><author><name sortKey="Yang, X D" uniqKey="Yang X">X.D. Yang</name></author><author><name sortKey="Zhou, M M" uniqKey="Zhou M">M.M. Zhou</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Chen, L F" uniqKey="Chen L">L.F. Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lin, Y J" uniqKey="Lin Y">Y.J. Lin</name></author><author><name sortKey="Umehara, T" uniqKey="Umehara T">T. Umehara</name></author><author><name sortKey="Inoue, M" uniqKey="Inoue M">M. Inoue</name></author><author><name sortKey="Saito, K" uniqKey="Saito K">K. Saito</name></author><author><name sortKey="Kigawa, T" uniqKey="Kigawa T">T. Kigawa</name></author><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Yokoyama, S" uniqKey="Yokoyama S">S. Yokoyama</name></author><author><name sortKey="Padmanabhan, B" uniqKey="Padmanabhan B">B. Padmanabhan</name></author><author><name sortKey="Guntert, P" uniqKey="Guntert P">P. Guntert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rahman, S" uniqKey="Rahman S">S. Rahman</name></author><author><name sortKey="Sowa, M E" uniqKey="Sowa M">M.E. Sowa</name></author><author><name sortKey="Ottinger, M" uniqKey="Ottinger M">M. Ottinger</name></author><author><name sortKey="Smith, J A" uniqKey="Smith J">J.A. Smith</name></author><author><name sortKey="Shi, Y" uniqKey="Shi Y">Y. Shi</name></author><author><name sortKey="Harper, J W" uniqKey="Harper J">J.W. Harper</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="You, J" uniqKey="You J">J. You</name></author><author><name sortKey="Croyle, J L" uniqKey="Croyle J">J.L. Croyle</name></author><author><name sortKey="Nishimura, A" uniqKey="Nishimura A">A. Nishimura</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bisgrove, D A" uniqKey="Bisgrove D">D.A. Bisgrove</name></author><author><name sortKey="Mahmoudi, T" uniqKey="Mahmoudi T">T. Mahmoudi</name></author><author><name sortKey="Henklein, P" uniqKey="Henklein P">P. Henklein</name></author><author><name sortKey="Verdin, E" uniqKey="Verdin E">E. Verdin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, S Y" uniqKey="Wu S">S.Y. Wu</name></author><author><name sortKey="Lee, A Y" uniqKey="Lee A">A.Y. Lee</name></author><author><name sortKey="Lai, H T" uniqKey="Lai H">H.T. Lai</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Chiang, C M" uniqKey="Chiang C">C.M. Chiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="French, C A" uniqKey="French C">C.A. French</name></author><author><name sortKey="Miyoshi, I" uniqKey="Miyoshi I">I. Miyoshi</name></author><author><name sortKey="Aster, J C" uniqKey="Aster J">J.C. Aster</name></author><author><name sortKey="Kubonishi, I" uniqKey="Kubonishi I">I. Kubonishi</name></author><author><name sortKey="Kroll, T G" uniqKey="Kroll T">T.G. Kroll</name></author><author><name sortKey="Dal Cin, P" uniqKey="Dal Cin P">P. Dal Cin</name></author><author><name sortKey="Vargas, S O" uniqKey="Vargas S">S.O. Vargas</name></author><author><name sortKey="Perez Atayde, A R" uniqKey="Perez Atayde A">A.R. Perez-Atayde</name></author><author><name sortKey="Fletcher, J A" uniqKey="Fletcher J">J.A. Fletcher</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reynoird, N" uniqKey="Reynoird N">N. Reynoird</name></author><author><name sortKey="Schwartz, B E" uniqKey="Schwartz B">B.E. Schwartz</name></author><author><name sortKey="Delvecchio, M" uniqKey="Delvecchio M">M. Delvecchio</name></author><author><name sortKey="Sadoul, K" uniqKey="Sadoul K">K. Sadoul</name></author><author><name sortKey="Meyers, D" uniqKey="Meyers D">D. Meyers</name></author><author><name sortKey="Mukherjee, C" uniqKey="Mukherjee C">C. Mukherjee</name></author><author><name sortKey="Caron, C" uniqKey="Caron C">C. Caron</name></author><author><name sortKey="Kimura, H" uniqKey="Kimura H">H. Kimura</name></author><author><name sortKey="Rousseaux, S" uniqKey="Rousseaux S">S. Rousseaux</name></author><author><name sortKey="Cole, P A" uniqKey="Cole P">P.A. Cole</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Filippakopoulos, P" uniqKey="Filippakopoulos P">P. Filippakopoulos</name></author><author><name sortKey="Qi, J" uniqKey="Qi J">J. Qi</name></author><author><name sortKey="Picaud, S" uniqKey="Picaud S">S. Picaud</name></author><author><name sortKey="Shen, Y" uniqKey="Shen Y">Y. Shen</name></author><author><name sortKey="Smith, W B" uniqKey="Smith W">W.B. Smith</name></author><author><name sortKey="Fedorov, O" uniqKey="Fedorov O">O. Fedorov</name></author><author><name sortKey="Morse, E M" uniqKey="Morse E">E.M. Morse</name></author><author><name sortKey="Keates, T" uniqKey="Keates T">T. Keates</name></author><author><name sortKey="Hickman, T T" uniqKey="Hickman T">T.T. Hickman</name></author><author><name sortKey="Felletar, I" uniqKey="Felletar I">I. Felletar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schwartz, B E" uniqKey="Schwartz B">B.E. Schwartz</name></author><author><name sortKey="Hofer, M D" uniqKey="Hofer M">M.D. Hofer</name></author><author><name sortKey="Lemieux, M E" uniqKey="Lemieux M">M.E. Lemieux</name></author><author><name sortKey="Bauer, D E" uniqKey="Bauer D">D.E. Bauer</name></author><author><name sortKey="Cameron, M J" uniqKey="Cameron M">M.J. Cameron</name></author><author><name sortKey="West, N H" uniqKey="West N">N.H. West</name></author><author><name sortKey="Agoston, E S" uniqKey="Agoston E">E.S. Agoston</name></author><author><name sortKey="Reynoird, N" uniqKey="Reynoird N">N. Reynoird</name></author><author><name sortKey="Khochbin, S" uniqKey="Khochbin S">S. Khochbin</name></author><author><name sortKey="Ince, T A" uniqKey="Ince T">T.A. Ince</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yan, J" uniqKey="Yan J">J. Yan</name></author><author><name sortKey="Diaz, J" uniqKey="Diaz J">J. Diaz</name></author><author><name sortKey="Jiao, J" uniqKey="Jiao J">J. Jiao</name></author><author><name sortKey="Wang, R" uniqKey="Wang R">R. Wang</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Crawford, N P S" uniqKey="Crawford N">N.P.S. Crawford</name></author><author><name sortKey="Alsarraj, J" uniqKey="Alsarraj J">J. Alsarraj</name></author><author><name sortKey="Lukes, L" uniqKey="Lukes L">L. Lukes</name></author><author><name sortKey="Walker, R C" uniqKey="Walker R">R.C. Walker</name></author><author><name sortKey="Officewala, J S" uniqKey="Officewala J">J.S. Officewala</name></author><author><name sortKey="Yang, H H" uniqKey="Yang H">H.H. Yang</name></author><author><name sortKey="Lee, M P" uniqKey="Lee M">M.P. Lee</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Hunter, K W" uniqKey="Hunter K">K.W. Hunter</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lockwood, W W" uniqKey="Lockwood W">W.W. Lockwood</name></author><author><name sortKey="Zejnullahu, K" uniqKey="Zejnullahu K">K. Zejnullahu</name></author><author><name sortKey="Bradner, J E" uniqKey="Bradner J">J.E. Bradner</name></author><author><name sortKey="Varmus, H" uniqKey="Varmus H">H. Varmus</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ott, C J" uniqKey="Ott C">C.J. Ott</name></author><author><name sortKey="Kopp, N" uniqKey="Kopp N">N. Kopp</name></author><author><name sortKey="Bird, L" uniqKey="Bird L">L. Bird</name></author><author><name sortKey="Paranal, R M" uniqKey="Paranal R">R.M. Paranal</name></author><author><name sortKey="Qi, J" uniqKey="Qi J">J. Qi</name></author><author><name sortKey="Bowman, T" uniqKey="Bowman T">T. Bowman</name></author><author><name sortKey="Rodig, S J" uniqKey="Rodig S">S.J. Rodig</name></author><author><name sortKey="Kung, A L" uniqKey="Kung A">A.L. Kung</name></author><author><name sortKey="Bradner, J E" uniqKey="Bradner J">J.E. Bradner</name></author><author><name sortKey="Weinstock, D M" uniqKey="Weinstock D">D.M. Weinstock</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dawson, M A" uniqKey="Dawson M">M.A. Dawson</name></author><author><name sortKey="Prinjha, R K" uniqKey="Prinjha R">R.K. Prinjha</name></author><author><name sortKey="Dittmann, A" uniqKey="Dittmann A">A. Dittmann</name></author><author><name sortKey="Giotopoulos, G" uniqKey="Giotopoulos G">G. Giotopoulos</name></author><author><name sortKey="Bantscheff, M" uniqKey="Bantscheff M">M. Bantscheff</name></author><author><name sortKey="Chan, W I" uniqKey="Chan W">W.I. Chan</name></author><author><name sortKey="Robson, S C" uniqKey="Robson S">S.C. Robson</name></author><author><name sortKey="Chung, C W" uniqKey="Chung C">C.W. Chung</name></author><author><name sortKey="Hopf, C" uniqKey="Hopf C">C. Hopf</name></author><author><name sortKey="Savitski, M M" uniqKey="Savitski M">M.M. Savitski</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Delmore, J E" uniqKey="Delmore J">J.E. Delmore</name></author><author><name sortKey="Issa, G C" uniqKey="Issa G">G.C. Issa</name></author><author><name sortKey="Lemieux, M E" uniqKey="Lemieux M">M.E. Lemieux</name></author><author><name sortKey="Rahl, P B" uniqKey="Rahl P">P.B. Rahl</name></author><author><name sortKey="Shi, J" uniqKey="Shi J">J. Shi</name></author><author><name sortKey="Jacobs, H M" uniqKey="Jacobs H">H.M. Jacobs</name></author><author><name sortKey="Kastritis, E" uniqKey="Kastritis E">E. Kastritis</name></author><author><name sortKey="Gilpatrick, T" uniqKey="Gilpatrick T">T. Gilpatrick</name></author><author><name sortKey="Paranal, R M" uniqKey="Paranal R">R.M. Paranal</name></author><author><name sortKey="Qi, J" uniqKey="Qi J">J. Qi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mertz, J A" uniqKey="Mertz J">J.A. Mertz</name></author><author><name sortKey="Conery, A R" uniqKey="Conery A">A.R. Conery</name></author><author><name sortKey="Bryant, B M" uniqKey="Bryant B">B.M. Bryant</name></author><author><name sortKey="Sandy, P" uniqKey="Sandy P">P. Sandy</name></author><author><name sortKey="Balasubramanian, S" uniqKey="Balasubramanian S">S. Balasubramanian</name></author><author><name sortKey="Mele, D A" uniqKey="Mele D">D.A. Mele</name></author><author><name sortKey="Bergeron, L" uniqKey="Bergeron L">L. Bergeron</name></author><author><name sortKey="Sims, R J" uniqKey="Sims R">R.J. Sims</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Olejnik Schmidt, A K" uniqKey="Olejnik Schmidt A">A.K. Olejnik-Schmidt</name></author><author><name sortKey="Schmidt, M T" uniqKey="Schmidt M">M.T. Schmidt</name></author><author><name sortKey="Kedzia, W" uniqKey="Kedzia W">W. Kedzia</name></author><author><name sortKey="Gozdzicka Jozefiak, A" uniqKey="Gozdzicka Jozefiak A">A. Gozdzicka-Jozefiak</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Baxter, M K" uniqKey="Baxter M">M.K. Baxter</name></author><author><name sortKey="Mcphillips, M G" uniqKey="Mcphillips M">M.G. McPhillips</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Platt, G M" uniqKey="Platt G">G.M. Platt</name></author><author><name sortKey="Simpson, G R" uniqKey="Simpson G">G.R. Simpson</name></author><author><name sortKey="Mittnacht, S" uniqKey="Mittnacht S">S. Mittnacht</name></author><author><name sortKey="Schulz, T F" uniqKey="Schulz T">T.F. Schulz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcphillips, M G" uniqKey="Mcphillips M">M.G. McPhillips</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lehman, C W" uniqKey="Lehman C">C.W. Lehman</name></author><author><name sortKey="Botchan, M R" uniqKey="Botchan M">M.R. Botchan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Abbate, E A" uniqKey="Abbate E">E.A. Abbate</name></author><author><name sortKey="Voitenleitner, C" uniqKey="Voitenleitner C">C. Voitenleitner</name></author><author><name sortKey="Botchan, M R" uniqKey="Botchan M">M.R. Botchan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcphillips, M G" uniqKey="Mcphillips M">M.G. McPhillips</name></author><author><name sortKey="Oliveira, J G" uniqKey="Oliveira J">J.G. Oliveira</name></author><author><name sortKey="Spindler, J E" uniqKey="Spindler J">J.E. Spindler</name></author><author><name sortKey="Mitra, R" uniqKey="Mitra R">R. Mitra</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ottinger, M" uniqKey="Ottinger M">M. Ottinger</name></author><author><name sortKey="Christalla, T" uniqKey="Christalla T">T. Christalla</name></author><author><name sortKey="Nathan, K" uniqKey="Nathan K">K. Nathan</name></author><author><name sortKey="Brinkmann, M M" uniqKey="Brinkmann M">M.M. Brinkmann</name></author><author><name sortKey="Viejo Borbolla, A" uniqKey="Viejo Borbolla A">A. Viejo-Borbolla</name></author><author><name sortKey="Schulz, T F" uniqKey="Schulz T">T.F. Schulz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="You, J" uniqKey="You J">J. You</name></author><author><name sortKey="Srinivasan, V" uniqKey="Srinivasan V">V. Srinivasan</name></author><author><name sortKey="Denis, G V" uniqKey="Denis G">G.V. Denis</name></author><author><name sortKey="Harrington, W J" uniqKey="Harrington W">W.J. Harrington</name></author><author><name sortKey="Ballestas, M E" uniqKey="Ballestas M">M.E. Ballestas</name></author><author><name sortKey="Kaye, K M" uniqKey="Kaye K">K.M. Kaye</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, A Y" uniqKey="Lee A">A.Y. Lee</name></author><author><name sortKey="Chiang, C M" uniqKey="Chiang C">C.M. Chiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gagnon, D" uniqKey="Gagnon D">D. Gagnon</name></author><author><name sortKey="Joubert, S" uniqKey="Joubert S">S. Joubert</name></author><author><name sortKey="Senechal, H" uniqKey="Senechal H">H. Senechal</name></author><author><name sortKey="Fradet Turcotte, A" uniqKey="Fradet Turcotte A">A. Fradet-Turcotte</name></author><author><name sortKey="Torre, S" uniqKey="Torre S">S. Torre</name></author><author><name sortKey="Archambault, J" uniqKey="Archambault J">J. Archambault</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zheng, G" uniqKey="Zheng G">G. Zheng</name></author><author><name sortKey="Schweiger, M R" uniqKey="Schweiger M">M.R. Schweiger</name></author><author><name sortKey="Martinez Noel, G" uniqKey="Martinez Noel G">G. Martinez-Noel</name></author><author><name sortKey="Zheng, L" uniqKey="Zheng L">L. Zheng</name></author><author><name sortKey="Smith, J A" uniqKey="Smith J">J.A. Smith</name></author><author><name sortKey="Harper, J W" uniqKey="Harper J">J.W. Harper</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Winokur, P L" uniqKey="Winokur P">P.L. Winokur</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sakai, H" uniqKey="Sakai H">H. Sakai</name></author><author><name sortKey="Yasugi, T" uniqKey="Yasugi T">T. Yasugi</name></author><author><name sortKey="Benson, J D" uniqKey="Benson J">J.D. Benson</name></author><author><name sortKey="Dowhanick, J J" uniqKey="Dowhanick J">J.J. Dowhanick</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Abroi, A" uniqKey="Abroi A">A. Abroi</name></author><author><name sortKey="Kurg, R" uniqKey="Kurg R">R. Kurg</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Breiding, D E" uniqKey="Breiding D">D.E. Breiding</name></author><author><name sortKey="Grossel, M J" uniqKey="Grossel M">M.J. Grossel</name></author><author><name sortKey="Androphy, E J" uniqKey="Androphy E">E.J. Androphy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ferguson, M F" uniqKey="Ferguson M">M.F. Ferguson</name></author><author><name sortKey="Botchan, M R" uniqKey="Botchan M">M.R. Botchan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cooper, C S" uniqKey="Cooper C">C.S. Cooper</name></author><author><name sortKey="Upmeyer, S N" uniqKey="Upmeyer S">S.N. Upmeyer</name></author><author><name sortKey="Winokur, P L" uniqKey="Winokur P">P.L. Winokur</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Antson, A A" uniqKey="Antson A">A.A. Antson</name></author><author><name sortKey="Burns, J E" uniqKey="Burns J">J.E. Burns</name></author><author><name sortKey="Moroz, O V" uniqKey="Moroz O">O.V. Moroz</name></author><author><name sortKey="Scott, D J" uniqKey="Scott D">D.J. Scott</name></author><author><name sortKey="Sanders, C M" uniqKey="Sanders C">C.M. Sanders</name></author><author><name sortKey="Bronstein, I B" uniqKey="Bronstein I">I.B. Bronstein</name></author><author><name sortKey="Dodson, G G" uniqKey="Dodson G">G.G. Dodson</name></author><author><name sortKey="Wilson, K S" uniqKey="Wilson K">K.S. Wilson</name></author><author><name sortKey="Maitland, N J" uniqKey="Maitland N">N.J. Maitland</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Senechal, H" uniqKey="Senechal H">H. Senechal</name></author><author><name sortKey="Poirier, G G" uniqKey="Poirier G">G.G. Poirier</name></author><author><name sortKey="Coulombe, B" uniqKey="Coulombe B">B. Coulombe</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author><author><name sortKey="Archambault, J" uniqKey="Archambault J">J. Archambault</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schweiger, M R" uniqKey="Schweiger M">M.R. Schweiger</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jha, S" uniqKey="Jha S">S. Jha</name></author><author><name sortKey="Vande, P S" uniqKey="Vande P">P.S. Vande</name></author><author><name sortKey="Banerjee, N S" uniqKey="Banerjee N">N.S. Banerjee</name></author><author><name sortKey="Dutta, A B" uniqKey="Dutta A">A.B. Dutta</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author><author><name sortKey="Dutta, A" uniqKey="Dutta A">A. Dutta</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kimura, A" uniqKey="Kimura A">A. Kimura</name></author><author><name sortKey="Horikoshi, M" uniqKey="Horikoshi M">M. Horikoshi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yan, J" uniqKey="Yan J">J. Yan</name></author><author><name sortKey="Li, Q" uniqKey="Li Q">Q. Li</name></author><author><name sortKey="Lievens, S" uniqKey="Lievens S">S. Lievens</name></author><author><name sortKey="Tavernier, J" uniqKey="Tavernier J">J. Tavernier</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bechtold, V" uniqKey="Bechtold V">V. Bechtold</name></author><author><name sortKey="Beard, P" uniqKey="Beard P">P. Beard</name></author><author><name sortKey="Raj, K" uniqKey="Raj K">K. Raj</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Baxter, M K" uniqKey="Baxter M">M.K. Baxter</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brokaw, J L" uniqKey="Brokaw J">J.L. Brokaw</name></author><author><name sortKey="Blanco, M" uniqKey="Blanco M">M. Blanco</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ilves, I" uniqKey="Ilves I">I. Ilves</name></author><author><name sortKey="Maemets, K" uniqKey="Maemets K">K. Maemets</name></author><author><name sortKey="Silla, T" uniqKey="Silla T">T. Silla</name></author><author><name sortKey="Janikson, K" uniqKey="Janikson K">K. Janikson</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Helfer, C M" uniqKey="Helfer C">C.M. Helfer</name></author><author><name sortKey="Pancholi, N" uniqKey="Pancholi N">N. Pancholi</name></author><author><name sortKey="Bradner, J E" uniqKey="Bradner J">J.E. Bradner</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sakakibara, N" uniqKey="Sakakibara N">N. Sakakibara</name></author><author><name sortKey="Chen, D" uniqKey="Chen D">D. Chen</name></author><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stubenrauch, F" uniqKey="Stubenrauch F">F. Stubenrauch</name></author><author><name sortKey="Colbert, A M" uniqKey="Colbert A">A.M. Colbert</name></author><author><name sortKey="Laimins, L A" uniqKey="Laimins L">L.A. Laimins</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Maruyama, T" uniqKey="Maruyama T">T. Maruyama</name></author><author><name sortKey="Farina, A" uniqKey="Farina A">A. Farina</name></author><author><name sortKey="Dey, A" uniqKey="Dey A">A. Dey</name></author><author><name sortKey="Cheong, J" uniqKey="Cheong J">J. Cheong</name></author><author><name sortKey="Bermudez, V P" uniqKey="Bermudez V">V.P. Bermudez</name></author><author><name sortKey="Tamura, T" uniqKey="Tamura T">T. Tamura</name></author><author><name sortKey="Sciortino, S" uniqKey="Sciortino S">S. Sciortino</name></author><author><name sortKey="Shuman, J" uniqKey="Shuman J">J. Shuman</name></author><author><name sortKey="Hurwitz, J" uniqKey="Hurwitz J">J. Hurwitz</name></author><author><name sortKey="Ozato, K" uniqKey="Ozato K">K. Ozato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Abroi, A" uniqKey="Abroi A">A. Abroi</name></author><author><name sortKey="Ilves, I" uniqKey="Ilves I">I. Ilves</name></author><author><name sortKey="Kivi, S" uniqKey="Kivi S">S. Kivi</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cardenas Mora, J" uniqKey="Cardenas Mora J">J. Cardenas-Mora</name></author><author><name sortKey="Spindler, J E" uniqKey="Spindler J">J.E. Spindler</name></author><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="You, J" uniqKey="You J">J. You</name></author><author><name sortKey="Schweiger, M R" uniqKey="Schweiger M">M.R. Schweiger</name></author><author><name sortKey="Howley, P M" uniqKey="Howley P">P.M. Howley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brannon, A R" uniqKey="Brannon A">A.R. Brannon</name></author><author><name sortKey="Maresca, J A" uniqKey="Maresca J">J.A. Maresca</name></author><author><name sortKey="Boeke, J D" uniqKey="Boeke J">J.D. Boeke</name></author><author><name sortKey="Basrai, M A" uniqKey="Basrai M">M.A. Basrai</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oliveira, J G" uniqKey="Oliveira J">J.G. Oliveira</name></author><author><name sortKey="Colf, L A" uniqKey="Colf L">L.A. Colf</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Poddar, A" uniqKey="Poddar A">A. Poddar</name></author><author><name sortKey="Reed, S C" uniqKey="Reed S">S.C. Reed</name></author><author><name sortKey="Mcphillips, M G" uniqKey="Mcphillips M">M.G. McPhillips</name></author><author><name sortKey="Spindler, J E" uniqKey="Spindler J">J.E. Spindler</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sekhar, V" uniqKey="Sekhar V">V. Sekhar</name></author><author><name sortKey="Reed, S C" uniqKey="Reed S">S.C. Reed</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sekhar, V" uniqKey="Sekhar V">V. Sekhar</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Woodard, C" uniqKey="Woodard C">C. Woodard</name></author><author><name sortKey="Shamay, M" uniqKey="Shamay M">M. Shamay</name></author><author><name sortKey="Liao, G" uniqKey="Liao G">G. Liao</name></author><author><name sortKey="Zhu, J" uniqKey="Zhu J">J. Zhu</name></author><author><name sortKey="Ng, A N" uniqKey="Ng A">A.N. Ng</name></author><author><name sortKey="Li, R" uniqKey="Li R">R. Li</name></author><author><name sortKey="Newman, R" uniqKey="Newman R">R. Newman</name></author><author><name sortKey="Rho, H S" uniqKey="Rho H">H.S. Rho</name></author><author><name sortKey="Hu, J" uniqKey="Hu J">J. Hu</name></author><author><name sortKey="Wan, J" uniqKey="Wan J">J. Wan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author><author><name sortKey="Van Doorslaer, K" uniqKey="Van Doorslaer K">K. van Doorslaer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Donaldson, M M" uniqKey="Donaldson M">M.M. Donaldson</name></author><author><name sortKey="Boner, W" uniqKey="Boner W">W. Boner</name></author><author><name sortKey="Morgan, I M" uniqKey="Morgan I">I.M. Morgan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dao, L D" uniqKey="Dao L">L.D. Dao</name></author><author><name sortKey="Duffy, A" uniqKey="Duffy A">A. Duffy</name></author><author><name sortKey="Van Tine, B A" uniqKey="Van Tine B">B.A. van Tine</name></author><author><name sortKey="Wu, S Y" uniqKey="Wu S">S.Y. Wu</name></author><author><name sortKey="Chiang, C M" uniqKey="Chiang C">C.M. Chiang</name></author><author><name sortKey="Broker, T R" uniqKey="Broker T">T.R. Broker</name></author><author><name sortKey="Chow, L T" uniqKey="Chow L">L.T. Chow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, T" uniqKey="Yu T">T. Yu</name></author><author><name sortKey="Peng, Y C" uniqKey="Peng Y">Y.C. Peng</name></author><author><name sortKey="Androphy, E J" uniqKey="Androphy E">E.J. Androphy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Parish, J L" uniqKey="Parish J">J.L. Parish</name></author><author><name sortKey="Bean, A M" uniqKey="Bean A">A.M. Bean</name></author><author><name sortKey="Park, R B" uniqKey="Park R">R.B. Park</name></author><author><name sortKey="Androphy, E J" uniqKey="Androphy E">E.J. Androphy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Sakakibara, N" uniqKey="Sakakibara N">N. Sakakibara</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Silla, T" uniqKey="Silla T">T. Silla</name></author><author><name sortKey="Mannik, A" uniqKey="Mannik A">A. Mannik</name></author><author><name sortKey="Ustav, M" uniqKey="Ustav M">M. Ustav</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jang, M K" uniqKey="Jang M">M.K. Jang</name></author><author><name sortKey="Kwon, D" uniqKey="Kwon D">D. Kwon</name></author><author><name sortKey="Mcbride, A A" uniqKey="Mcbride A">A.A. McBride</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weidner Glunde, M" uniqKey="Weidner Glunde M">M. Weidner-Glunde</name></author><author><name sortKey="Ottinger, M" uniqKey="Ottinger M">M. Ottinger</name></author><author><name sortKey="Schulz, T F" uniqKey="Schulz T">T.F. Schulz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lin, A" uniqKey="Lin A">A. Lin</name></author><author><name sortKey="Wang, S" uniqKey="Wang S">S. Wang</name></author><author><name sortKey="Nguyen, T" uniqKey="Nguyen T">T. Nguyen</name></author><author><name sortKey="Shire, K" uniqKey="Shire K">K. Shire</name></author><author><name sortKey="Frappier, L" uniqKey="Frappier L">L. Frappier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Viejo Borbolla, A" uniqKey="Viejo Borbolla A">A. Viejo-Borbolla</name></author><author><name sortKey="Kati, E" uniqKey="Kati E">E. Kati</name></author><author><name sortKey="Sheldon, J A" uniqKey="Sheldon J">J.A. Sheldon</name></author><author><name sortKey="Nathan, K" uniqKey="Nathan K">K. Nathan</name></author><author><name sortKey="Mattsson, K" uniqKey="Mattsson K">K. Mattsson</name></author><author><name sortKey="Szekely, L" uniqKey="Szekely L">L. Szekely</name></author><author><name sortKey="Schulz, T F" uniqKey="Schulz T">T.F. Schulz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Schowalter, R M" uniqKey="Schowalter R">R.M. Schowalter</name></author><author><name sortKey="Jiao, J" uniqKey="Jiao J">J. Jiao</name></author><author><name sortKey="Buck, C B" uniqKey="Buck C">C.B. Buck</name></author><author><name sortKey="You, J" uniqKey="You J">J. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, Z" uniqKey="Li Z">Z. Li</name></author><author><name sortKey="Guo, J" uniqKey="Guo J">J. Guo</name></author><author><name sortKey="Wu, Y" uniqKey="Wu Y">Y. Wu</name></author><author><name sortKey="Zhou, Q" uniqKey="Zhou Q">Q. Zhou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Boehm, D" uniqKey="Boehm D">D. Boehm</name></author><author><name sortKey="Calvanese, V" uniqKey="Calvanese V">V. Calvanese</name></author><author><name sortKey="Dar, R D" uniqKey="Dar R">R.D. Dar</name></author><author><name sortKey="Xing, S" uniqKey="Xing S">S. Xing</name></author><author><name sortKey="Schroeder, S" uniqKey="Schroeder S">S. Schroeder</name></author><author><name sortKey="Martins, L" uniqKey="Martins L">L. Martins</name></author><author><name sortKey="Aull, K" uniqKey="Aull K">K. Aull</name></author><author><name sortKey="Li, P C" uniqKey="Li P">P.C. Li</name></author><author><name sortKey="Planelles, V" uniqKey="Planelles V">V. Planelles</name></author><author><name sortKey="Bradner, J E" uniqKey="Bradner J">J.E. Bradner</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhu, J" uniqKey="Zhu J">J. Zhu</name></author><author><name sortKey="Gaiha, G D" uniqKey="Gaiha G">G.D. Gaiha</name></author><author><name sortKey="John, S P" uniqKey="John S">S.P. John</name></author><author><name sortKey="Pertel, T" uniqKey="Pertel T">T. Pertel</name></author><author><name sortKey="Chin, C R" uniqKey="Chin C">C.R. Chin</name></author><author><name sortKey="Gao, G" uniqKey="Gao G">G. Gao</name></author><author><name sortKey="Qu, H" uniqKey="Qu H">H. Qu</name></author><author><name sortKey="Walker, B D" uniqKey="Walker B">B.D. Walker</name></author><author><name sortKey="Elledge, S J" uniqKey="Elledge S">S.J. Elledge</name></author><author><name sortKey="Brass, A L" uniqKey="Brass A">A.L. Brass</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Banerjee, C" uniqKey="Banerjee C">C. Banerjee</name></author><author><name sortKey="Archin, N" uniqKey="Archin N">N. Archin</name></author><author><name sortKey="Michaels, D" uniqKey="Michaels D">D. Michaels</name></author><author><name sortKey="Belkina, A C" uniqKey="Belkina A">A.C. Belkina</name></author><author><name sortKey="Denis, G V" uniqKey="Denis G">G.V. Denis</name></author><author><name sortKey="Bradner, J" uniqKey="Bradner J">J. Bradner</name></author><author><name sortKey="Sebastiani, P" uniqKey="Sebastiani P">P. Sebastiani</name></author><author><name sortKey="Margolis, D M" uniqKey="Margolis D">D.M. Margolis</name></author><author><name sortKey="Montano, M" uniqKey="Montano M">M. Montano</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Viruses</journal-id><journal-id journal-id-type="iso-abbrev">Viruses</journal-id><journal-id journal-id-type="publisher-id">viruses</journal-id><journal-title-group><journal-title>Viruses</journal-title></journal-title-group><issn pub-type="epub">1999-4915</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23722886</article-id><article-id pub-id-type="pmc">3717712</article-id><article-id pub-id-type="doi">10.3390/v5061374</article-id><article-id pub-id-type="publisher-id">viruses-05-01374</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Current Understanding of the Role of the Brd4 Protein in the Papillomavirus Lifecycle</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>McBride</surname><given-names>Alison A.</given-names></name><xref rid="c1-viruses-05-01374" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Jang</surname><given-names>Moon Kyoo</given-names></name></contrib></contrib-group><aff id="af1-viruses-05-01374">Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA; E-Mail:<email>jangmk@niaid.nih.gov</email></aff><author-notes><corresp id="c1-viruses-05-01374"><label>*</label> Author to whom correspondence should be addressed; E-Mail: <email>amcbride@nih.gov</email>; Tel.: +1-301-496-1370.</corresp></author-notes><pub-date pub-type="epub"><day>30</day><month>5</month><year>2013</year></pub-date><pub-date pub-type="collection"><month>6</month><year>2013</year></pub-date><volume>5</volume><issue>6</issue><fpage>1374</fpage><lpage>1394</lpage><history><date date-type="received"><day>02</day><month>4</month><year>2013</year></date><date date-type="rev-recd"><day>21</day><month>5</month><year>2013</year></date><date date-type="accepted"><day>21</day><month>5</month><year>2013</year></date></history><permissions><copyright-statement>© 2013 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement><copyright-year>2013</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/3.0/"><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/3.0/">http://creativecommons.org/licenses/by/3.0/</ext-link>).</license-p></license></permissions><abstract><p>The Brd4 protein is an epigenetic reader that is central to regulation of cellular transcription and mitotic bookmarking. The transcription and replication proteins of many viruses interact with Brd4. We describe the multiple roles of Brd4 in the papillomavirus lifecycle. </p></abstract><kwd-group><kwd>Brd4</kwd><kwd>BET protein</kwd><kwd>HPV</kwd><kwd>papillomavirus</kwd><kwd>transcription</kwd><kwd>chromatin</kwd><kwd>replication</kwd><kwd>tethering</kwd><kwd>partitioning</kwd><kwd>bromodomain</kwd></kwd-group></article-meta></front><body><sec><title>1. Introduction</title><p>Papillomaviruses (PVs) are an ancient group of viruses that have coevolved along with their hosts for millions of years. Each viral type infects only a particular host species and is trophic for a specific anatomical niche in the stratified epithelium of the skin or mucosa of the host. Papillomavirus infection is persistent and results in clinical outcomes, such as asymptomatic infection, verrucae, plantar and filiform warts and condylomata acuminata. A subset of oncogenic HPVs is associated with carcinomas of the oropharyngeal and anogenital tracts [<xref ref-type="bibr" rid="B1-viruses-05-01374">1</xref>,<xref ref-type="bibr" rid="B2-viruses-05-01374">2</xref>,<xref ref-type="bibr" rid="B3-viruses-05-01374">3</xref>]. Despite the diversity of pathogenesis associated with papillomavirus infection, all papillomaviruses have similar small dsDNA genomes of approximately 8 kbp (see <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>), and each encodes only six to eight genes. Papillomaviruses rely on hijacking and manipulating host factors to maintain their lifestyle. </p><fig id="viruses-05-01374-f001" position="float"><label>Figure 1</label><caption><p>HPV18 genome. The circular dsDNA genome of HPV18 (7,857 bp) is shown. Viral open reading frames are depicted as red arrows. The URR (upstream regulatory region) is expanded to show transcription and replication regulatory elements. Binding sites for the E2 protein (cyan circles) and the E1 binding site (blue rectangle) are shown. The early promoter and replication origin (ori) are indicated. </p></caption><graphic xlink:href="viruses-05-01374-g001"></graphic></fig><p>One key, cellular regulatory protein hijacked by all papillomaviruses (and other viral families) is a cellular chromatin binding protein, Brd4. Brd4 is an essential cellular protein that binds and marks chromatin to regulate several transcriptional processes. In this review, we will summarize the current knowledge pertaining to the role of Brd4 in papillomavirus infections. </p></sec><sec><title>2. Papillomaviruses</title><sec><title>2.1. The Papillomavirus Lifecycle</title><p>The stratified epithelium of the skin or mucosa consists of several layers of keratinocytes in various stages of differentiation, overlying the basal layer of proliferative cells. Papillomaviruses gain access to cells in the basal layer through a microabrasion. They infect these keratinocytes, induce their proliferation by expression of the viral E7 protein and establish a persistent infection therein. The viral genome is maintained as a low copy, extrachromosomal element in the nucleus of these cells, and only low levels of viral gene products are produced. When the infected cells divide, some of the daughter cells begin the process of stratification and differentiation and progress towards the surface of the epithelium. The papillomavirus lifecycle is finely tuned to this process of differentiation; viral transcription and replication switches from early to late modes as the cell differentiates. Vegetative viral DNA replication is initiated in the mid-layers of differentiated cells, and capsid synthesis is confined to the most differentiated layers of cells.</p></sec><sec><title>2.2. Viral Transcription</title><p>Papillomavirus genomes can be divided into three regions (see <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>). The upstream regulatory region (URR) contains transcriptional enhancers and promoters and the origin of replication. The early region encodes the E (early) proteins that are expressed at early and intermediate stages of infection. Last is the late region that contains the L (late) genes. In the most undifferentiated cells, viral RNAs are transcribed from the early promoter, terminate at the early polyadenylation site (pAE) and encode the E6, E7, E1, E2, E4 and E5 proteins (reviewed in [<xref ref-type="bibr" rid="B4-viruses-05-01374">4</xref>]). As the cells progress through differentiation, the late promoter is activated, resulting in an intermediate class of transcripts that use the late promoter and the early polyadenylation signal. These transcripts encode high levels of the E4, E1 and E2, the latter two being required for high level vegetative viral DNA replication in the mid‑layers of the epithelium. Exclusively late transcripts are expressed at an even later stage of differentiation; they use both the late promoter and late polyadenylation signal (pAL) and encode the L1 and L2 capsid proteins. Complex patterns of viral mRNA species are generated by the use of alternative splicing and viral gene expression is highly regulated by differential splicing and polyadenylation (reviewed in [<xref ref-type="bibr" rid="B4-viruses-05-01374">4</xref>]). </p><p>The E2 protein is the primary regulator of early viral transcription [<xref ref-type="bibr" rid="B5-viruses-05-01374">5</xref>]. E2 consists of a conserved amino terminal “transactivation” domain linked to a C-terminal DNA binding/dimerization domain by a poorly conserved linker (see <xref ref-type="fig" rid="viruses-05-01374-f002">Figure 2</xref>) [<xref ref-type="bibr" rid="B6-viruses-05-01374">6</xref>]. E2 specifically binds to a consensus sequence of ACCGNNNNCGGT, several copies of which are located in the viral URR [<xref ref-type="bibr" rid="B7-viruses-05-01374">7</xref>] (see <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>). E2 can activate transcription from certain viral promoters [<xref ref-type="bibr" rid="B5-viruses-05-01374">5</xref>,<xref ref-type="bibr" rid="B8-viruses-05-01374">8</xref>,<xref ref-type="bibr" rid="B9-viruses-05-01374">9</xref>,<xref ref-type="bibr" rid="B10-viruses-05-01374">10</xref>], but the early viral promoter in the well-studied, oncogenic alpha-PVs is primarily repressed by E2 [<xref ref-type="bibr" rid="B11-viruses-05-01374">11</xref>,<xref ref-type="bibr" rid="B12-viruses-05-01374">12</xref>,<xref ref-type="bibr" rid="B13-viruses-05-01374">13</xref>]. Early studies showed that E2 could repress the early promoter by sterically hindering the association of TBP and Sp1 with promoter elements adjacent to E2 binding sites 1 and 2 [<xref ref-type="bibr" rid="B14-viruses-05-01374">14</xref>,<xref ref-type="bibr" rid="B15-viruses-05-01374">15</xref>,<xref ref-type="bibr" rid="B16-viruses-05-01374">16</xref>]. Subsequent studies have shown that much of this E2-mediated repression is mediated through interaction with factors that modulate cellular chromatin processes [<xref ref-type="bibr" rid="B17-viruses-05-01374">17</xref>,<xref ref-type="bibr" rid="B18-viruses-05-01374">18</xref>,<xref ref-type="bibr" rid="B19-viruses-05-01374">19</xref>,<xref ref-type="bibr" rid="B20-viruses-05-01374">20</xref>]. Disruption of E2-mediated repression (often due to HPV integration) results in increased expression of the E6 and E7 oncogenes [<xref ref-type="bibr" rid="B11-viruses-05-01374">11</xref>,<xref ref-type="bibr" rid="B12-viruses-05-01374">12</xref>,<xref ref-type="bibr" rid="B21-viruses-05-01374">21</xref>]. In fact, reintroduction of the E2 protein into cervical cancer-derived lines (such as HeLa) leads to rapid senescence, as viability of these cells is completely dependent on E6 and E7 expression [<xref ref-type="bibr" rid="B22-viruses-05-01374">22</xref>,<xref ref-type="bibr" rid="B23-viruses-05-01374">23</xref>,<xref ref-type="bibr" rid="B24-viruses-05-01374">24</xref>].</p><p>Shorter forms of the E2 protein that are lacking the transactivation domain also repress HPV transcription, in part by competing for binding to E2 binding motifs [<xref ref-type="bibr" rid="B25-viruses-05-01374">25</xref>,<xref ref-type="bibr" rid="B26-viruses-05-01374">26</xref>]. One of the best characterized is the E8^E2 protein (encoded from a spliced transcript), which also represses through the recruitment of chromatin-associated repressive factors [<xref ref-type="bibr" rid="B27-viruses-05-01374">27</xref>]. As described in detail below, E2 interacts with the Brd4 protein, and this association is pivotal to transcriptional regulation of HPVs.</p><fig id="viruses-05-01374-f002" position="float"><label>Figure 2</label><caption><p>Structure of the papillomavirus E2 protein. The two domains of the E2 protein are shown. The transactivation domain structure is of HPV16 E2 bound to the Brd4 C-terminal motif (CTM). The Brd4 C-terminal peptide (residues 1343–1362) is shown in magenta. This structure is from the pdb file, 2NNU. The DNA binding domain is of the HPV18 DNA binding domain bound to DNA (shown in light purple) from the pdb file 1JJ4. </p></caption><graphic xlink:href="viruses-05-01374-g002"></graphic></fig></sec><sec><title>2.3. Disruption of E2 Function by HPV Integration</title><p>In the majority of HPV associated cancers, the HPV genome is integrated into the host genome (reviewed in [<xref ref-type="bibr" rid="B28-viruses-05-01374">28</xref>]). The viral genome is most often integrated in such a way as to disrupt the E2 gene and, thus, alleviate transcriptional repression of the early viral promoter [<xref ref-type="bibr" rid="B22-viruses-05-01374">22</xref>,<xref ref-type="bibr" rid="B23-viruses-05-01374">23</xref>,<xref ref-type="bibr" rid="B24-viruses-05-01374">24</xref>,<xref ref-type="bibr" rid="B29-viruses-05-01374">29</xref>]. In turn, this causes dysregulation of the E6 and E7 oncogenes and promotes malignant progression [<xref ref-type="bibr" rid="B30-viruses-05-01374">30</xref>]. </p></sec><sec><title>2.4. Viral Replication</title><p>Papillomavirus replication requires the E1 protein, the E2 protein and the origin of replication [<xref ref-type="bibr" rid="B31-viruses-05-01374">31</xref>,<xref ref-type="bibr" rid="B32-viruses-05-01374">32</xref>,<xref ref-type="bibr" rid="B33-viruses-05-01374">33</xref>]. E1 is the primary replication protein, an ATP-dependent helicase that binds specifically to the origin and unwinds it in a bidirectional manner to permit access by the cellular replication machinery (reviewed in [<xref ref-type="bibr" rid="B34-viruses-05-01374">34</xref>]). E2 functions to load the E1 helicase onto the origin [<xref ref-type="bibr" rid="B35-viruses-05-01374">35</xref>]. As depicted in <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>, the minimal origin consists of the E1 binding site flanked by E2 binding sites and overlaps elements regulating the early promoter. </p><p>There are three modes of viral replication in the viral lifecycle. The first is a limited amplification that occurs when the virus particle infects a basal keratinocyte. The virus must undergo a few rounds of unlicensed DNA replication to establish the genome as a low copy, nuclear, extrachromosomal element. This phase requires E1, E2 and the minimal replication origin. The second phase of replication maintains the viral genome at a low copy number during division of the proliferating basal cells. This also requires E1, E2 and the minimal origin of replication, but there is an additional requirement for additional E2 binding sites in <italic>cis</italic> to the origin, thus implicating the E2 protein in maintenance replication [<xref ref-type="bibr" rid="B36-viruses-05-01374">36</xref>]. Subsequent studies showed that the role of E2 was to tether the viral genomes to the host chromatin [<xref ref-type="bibr" rid="B37-viruses-05-01374">37</xref>,<xref ref-type="bibr" rid="B38-viruses-05-01374">38</xref>,<xref ref-type="bibr" rid="B39-viruses-05-01374">39</xref>]. The interaction of E2 with Brd4 is crucial for the tethering function of many papillomaviruses and will be discussed in detail below. Further investigation showed that the E1 protein was not always necessary for maintenance replication and, presumably, in this situation viral replication, is initiated by cellular factors, while the genome is retained by the E2 protein [<xref ref-type="bibr" rid="B40-viruses-05-01374">40</xref>,<xref ref-type="bibr" rid="B41-viruses-05-01374">41</xref>]. </p><p>The third phase of replication is vegetative amplification, when progeny virions are produced in large numbers in differentiated cells. This requires the E1 and E2 proteins, and their expression is upregulated in differentiated cells [<xref ref-type="bibr" rid="B42-viruses-05-01374">42</xref>,<xref ref-type="bibr" rid="B43-viruses-05-01374">43</xref>]. There is evidence that the mode of replication changes in differentiated cells [<xref ref-type="bibr" rid="B44-viruses-05-01374">44</xref>], and incorporation of Rad51 into replication foci indicates that the virus may replicate using a recombination directed replication mechanism [<xref ref-type="bibr" rid="B45-viruses-05-01374">45</xref>,<xref ref-type="bibr" rid="B46-viruses-05-01374">46</xref>]. Furthermore, the cellular ataxia telangiectasia mutated (ATM) DNA damage response pathway is required for vegetative replication in differentiated cells [<xref ref-type="bibr" rid="B47-viruses-05-01374">47</xref>]. Nuclear foci formed by either expression of the E1 and E2 proteins [<xref ref-type="bibr" rid="B48-viruses-05-01374">48</xref>,<xref ref-type="bibr" rid="B49-viruses-05-01374">49</xref>,<xref ref-type="bibr" rid="B50-viruses-05-01374">50</xref>,<xref ref-type="bibr" rid="B51-viruses-05-01374">51</xref>] or the replicating viral genome [<xref ref-type="bibr" rid="B46-viruses-05-01374">46</xref>,<xref ref-type="bibr" rid="B47-viruses-05-01374">47</xref>] recruit multiple cellular proteins required for the cellular DNA damage response and repair pathways.</p></sec><sec><title>2.5. Differences in Transcription and Replication among Papillomaviruses</title><p>To date, there are over 240 named papillomavirus genomes that have been classified into 37 different genera [<xref ref-type="bibr" rid="B52-viruses-05-01374">52</xref>]. The best studied are human viruses from the alpha and beta genera that infect primarily the mucosa and skin, respectively. The human mu virus, HPV1, and the ungulate delta virus, BPV1, are also well characterized. While each of these viruses has a similar organization of genes to that of HPV18 (an alpha-PV) shown in <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>, the number and position of the E2 binding sites can vary considerably. BPV1 has 11 E2 binding sites in the URR and six elsewhere in the genome [<xref ref-type="bibr" rid="B53-viruses-05-01374">53</xref>], while most human alpha viruses have only the four E2 sites shown in <xref ref-type="fig" rid="viruses-05-01374-f001">Figure 1</xref>. In BPV1 E2 is primarily an activator of transcription [<xref ref-type="bibr" rid="B5-viruses-05-01374">5</xref>], while E2 predominantly represses the major early promoter of alpha-PVs.</p><p>All viruses require the minimal replication origin and the E1 and E2 proteins to initiate replication, but the requirements for maintenance replication are more complex. E2 binding sites are essential for initiation of replication and for transcriptional regulation making it very difficult to separate and elucidate the role of individual sites in maintenance replication of the viral genome. Maintenance replication is best understood for BPV1, where it has been shown that at least eight E2 binding sites are required for persistent replication [<xref ref-type="bibr" rid="B36-viruses-05-01374">36</xref>]. In the alpha-PV HPV31, only three of the four E2 binding sites are required for maintenance replication of the viral genome [<xref ref-type="bibr" rid="B54-viruses-05-01374">54</xref>]. In agreement with this finding, using a novel complementation assay, we find that a region encompassing the 3’ half of the URR of HPV18 (containing E2 binding sites 1–3) is sufficient for long-term maintenance in the presence of the E1 and E2 proteins [<xref ref-type="bibr" rid="B55-viruses-05-01374">55</xref>]. </p></sec></sec><sec><title>3. The Brd4 Protein</title><sec><title>3.1. Brd4 Structure and Function</title><p>Brd4 was first described as an unusual chromatin binding factor that remained bound to chromosomes throughout mitosis [<xref ref-type="bibr" rid="B56-viruses-05-01374">56</xref>]. It is a member the BET (bromodomain and extra-terminal domain) family of chromatin binding proteins and, therefore, its name was changed from MCAP (mitotic chromosome-associated protein) to bromodomain containing protein 4 (Brd4) [<xref ref-type="bibr" rid="B57-viruses-05-01374">57</xref>]. Brd4 is an essential protein [<xref ref-type="bibr" rid="B58-viruses-05-01374">58</xref>] that is ubiquitous in proliferating cells. The tandem bromodomains of Brd4 interact with acetylated tails of H3 and H4 histones [<xref ref-type="bibr" rid="B59-viruses-05-01374">59</xref>], and Brd4 has been shown to be a mitotic bookmark that marks genes, which are expressed shortly after mitotic exit [<xref ref-type="bibr" rid="B60-viruses-05-01374">60</xref>,<xref ref-type="bibr" rid="B61-viruses-05-01374">61</xref>]. Brd4 decompacts chromatin and recruits transcriptional initiation and elongation factors to rapidly activate early G1 genes post-mitosis, as well as later in interphase [<xref ref-type="bibr" rid="B62-viruses-05-01374">62</xref>]. Brd4 recruits the transcriptional elongation factor, p-TEFb, to promoters to enhance phosphorylation of the C-terminal tail (CTD) of RNA polymerase II promoters to stimulate transcription [<xref ref-type="bibr" rid="B63-viruses-05-01374">63</xref>,<xref ref-type="bibr" rid="B64-viruses-05-01374">64</xref>]. Brd4 further promotes transcription by directly phosphorylating the RNA polymerase II CTD [<xref ref-type="bibr" rid="B65-viruses-05-01374">65</xref>]. This fundamental role of Brd4 in transcriptional regulation places it at the center of many diverse biological activities. </p><p>The Brd4 gene encodes two proteins; the short form of Brd4 contains the two bromodomains and the extra-terminal (ET) region (important for many protein-protein interactions), while the longer form of Brd4 has an additional, long unique C-terminal region (see <xref ref-type="fig" rid="viruses-05-01374-f003">Figure 3</xref>). The structures of both bromodomains and the ET domains have been solved [<xref ref-type="bibr" rid="B66-viruses-05-01374">66</xref>,<xref ref-type="bibr" rid="B67-viruses-05-01374">67</xref>]. The bromodomains bind to specific acetylated lysines on H3 and H4, but BD2 (bromodomain 2) can also interact with acetylated residues in other proteins, such as cyclin T1 (the p-TEFb subunit) and the relA subunit of NFκB [<xref ref-type="bibr" rid="B67-viruses-05-01374">67</xref>,<xref ref-type="bibr" rid="B68-viruses-05-01374">68</xref>,<xref ref-type="bibr" rid="B69-viruses-05-01374">69</xref>]. </p><p>The extra-terminal domain consists of three alpha-helices, and it seems to be a site of protein-protein interaction [<xref ref-type="bibr" rid="B70-viruses-05-01374">70</xref>]. It binds proteins involved in transcriptional regulation, such as NSD3 (also known as WHSC1L1), a histone methyl transferase, JMJD6, a histone demethylase, and CHD4, a component of the NuRD (nuclear remodeling and deacetylase) repressor complex. Thus, Brd4 has the potential to assemble multifaceted positive and negative regulatory complexes on promoters [<xref ref-type="bibr" rid="B71-viruses-05-01374">71</xref>]. </p><p>The function of the C-terminal region is not well-characterized, except for the last 100 amino acids, which is important for interacting with the papillomavirus E2 protein [<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>] and with p-TEFb [<xref ref-type="bibr" rid="B73-viruses-05-01374">73</xref>] (see <xref ref-type="fig" rid="viruses-05-01374-f003">Figure 3</xref>). Thus, p-TEFb interacts with two independent regions of the Brd4 protein [<xref ref-type="bibr" rid="B68-viruses-05-01374">68</xref>]. </p><fig id="viruses-05-01374-f003" position="float"><label>Figure 3</label><caption><p>Structure and function of the Brd4 protein. (<bold>a</bold>) Domains of the Brd4 protein. The domains shown are BD1 (bromodomain I: residues 58–169); BD2 (bromodomain 2: residues 349–461); NPS (N-terminal cluster of phosphorylation sites: residues 484–503); BID (basic residue enriched interaction domain: residues 524–579); ET (extra-terminal domain: residues 600–678); PDID (phosphorylation dependent interaction domain: residues 287–530); SEED (Ser/Glu/Asp-rich region: residues 695–720); CTM (C-terminal motif: residues 1325–1362); CTD (dominant negative domain of Brd4: residues 1047–1362) and PID (pTEF binding region: residues 1209–1362) [<xref ref-type="bibr" rid="B73-viruses-05-01374">73</xref>]. (<bold>b</bold>) Viral and cellular interacting partners of Brd4. See text for references.</p></caption><graphic xlink:href="viruses-05-01374-g003"></graphic></fig><p>p53 has also recently been shown to be a binding partner of Brd4, and analysis of this interaction revealed a conformational switch in Brd4 structure and protein-protein interactions modulated by CK2 phosphorylation [<xref ref-type="bibr" rid="B74-viruses-05-01374">74</xref>]. A region between the second bromodomain and the ET domain contains two interaction regions, BID (basic residue enriched interaction domain) and NPS (N-terminal cluster of phosphorylation sites), that modulate this switch. When unphosphorylated, the NPS region interacts with the PDID (phosphorylation dependent interaction domain) that encompasses bromodomain 2, thus preventing Brd4 from binding to acetylated histones (see <xref ref-type="fig" rid="viruses-05-01374-f003">Figure 3</xref>). p53 binds to the BID region when Brd4 is unphosphorylated. Upon phosphorylation of NPS, p53 is released from binding to BID, and both p53 and BID now associate with phosphorylated NPS, thus exposing the bromodomain 2 in PDID and activating the complex [<xref ref-type="bibr" rid="B74-viruses-05-01374">74</xref>]. </p></sec><sec><title>3.2. Association of Brd4 with Disease</title><p>The first association of Brd4 with human disease was the discovery that the aggressive NUT midline carcinoma (NMC) was due to a translocation (t(15;19)(q13;p13)), resulting in the fusion of Brd4 with NUT (nuclear protein in testes) [<xref ref-type="bibr" rid="B75-viruses-05-01374">75</xref>]. The NUT protein recruits the histone acetyl transferase, p300, resulting in a feed-forward loop of histone acetylation and Brd4-NUT recruitment, which gives rise to hyperacetylated, but inactive, chromosomal foci [<xref ref-type="bibr" rid="B76-viruses-05-01374">76</xref>]. Sequestration of Brd4 and p‑TEFb to these foci promotes proliferation of Brd4-NUT cells. This can be reversed and differentiation restored, by siRNA to Brd4, by histone deacetylase inhibitors that promote global acetylation and by BET protein-specific histone mimics [<xref ref-type="bibr" rid="B77-viruses-05-01374">77</xref>,<xref ref-type="bibr" rid="B78-viruses-05-01374">78</xref>,<xref ref-type="bibr" rid="B79-viruses-05-01374">79</xref>]. </p><p>Brd4 is also a modifier of breast cancer metastasis [<xref ref-type="bibr" rid="B80-viruses-05-01374">80</xref>] and a promising target for several cancers, because of its fundamental role in transcriptional processes. Targeted inhibition of BET bromodomain binding is potentially therapeutic for glioblastoma, lung adenocarcinoma, ALL (acute lymphoblastic leukemia) and MLL (mixed-lineage leukemia) [<xref ref-type="bibr" rid="B81-viruses-05-01374">81</xref>,<xref ref-type="bibr" rid="B82-viruses-05-01374">82</xref>,<xref ref-type="bibr" rid="B83-viruses-05-01374">83</xref>,<xref ref-type="bibr" rid="B84-viruses-05-01374">84</xref>,<xref ref-type="bibr" rid="B85-viruses-05-01374">85</xref>]. </p></sec></sec><sec><title>4. Brd4 and Papillomaviruses</title><p>Brd4 was discovered to be a major interactor of the papillomavirus E2 protein by proteomic analyses [<xref ref-type="bibr" rid="B20-viruses-05-01374">20</xref>,<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>], yeast two hybrid screening [<xref ref-type="bibr" rid="B86-viruses-05-01374">86</xref>]. It was also investigated as an E2 target, because the analogous tethering protein in KSHV (LANA) interacts with the BET family member, Brd2 [<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>,<xref ref-type="bibr" rid="B88-viruses-05-01374">88</xref>,<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>]. The E2 protein had previously been shown to bind and tether viral genomes to host mitotic chromosomes [<xref ref-type="bibr" rid="B37-viruses-05-01374">37</xref>,<xref ref-type="bibr" rid="B38-viruses-05-01374">38</xref>,<xref ref-type="bibr" rid="B39-viruses-05-01374">39</xref>,<xref ref-type="bibr" rid="B90-viruses-05-01374">90</xref>], and the Brd4 protein colocalized completely with these chromatin bound speckles of E2 [<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>,<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>,<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>,<xref ref-type="bibr" rid="B91-viruses-05-01374">91</xref>]. The E2 protein is a multifunctional protein involved in papillomavirus transcription, maintenance and partitioning of extrachromosomal viral genomes and initiation of viral DNA replication. Many subsequent studies have dissected the role of Brd4 in each of these processes. </p><sec><title>4.1. Interaction between Papillomavirus E2 and Brd4 Proteins</title><p>The Brd4 protein binds primarily to the transactivation domain of the E2 proteins (see <xref ref-type="fig" rid="viruses-05-01374-f002">Figure 2</xref>) [<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>]. The transactivation domain contacts a peptide at the extreme C-terminus of the Brd4 protein [<xref ref-type="bibr" rid="B91-viruses-05-01374">91</xref>], and a C-terminal domain of Brd4 (CTD; residues 1047–1362) has proven useful as a dominant-negative inhibitor of the E2-Brd4 interaction [<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>]. The region of the E2 transactivation domain that makes contact with the Brd4 CTD is highly conserved; yet, there is a wide range of binding affinities between Brd4 and E2 proteins from different papillomaviruses [<xref ref-type="bibr" rid="B92-viruses-05-01374">92</xref>]. The C-terminal DNA binding domain of E2 does not seem necessary for Brd4 binding, but the dimerization function of this domain greatly increases E2-Brd4 binding both <italic>in vivo</italic> and <italic>in vitro</italic>. There are hints that there may be additional contacts between E2 and Brd4: HPV11 E2 binds to the Brd4 CTD, but also to a region encompassing bromodomain 2 (BD2). The DNA binding domain of the KSHV LANA protein (a tethering protein analogous to E2 and with a DNA binding domain of similar structure) interacts with the ET domain of Brd4 [<xref ref-type="bibr" rid="B93-viruses-05-01374">93</xref>,<xref ref-type="bibr" rid="B94-viruses-05-01374">94</xref>]. It is likely that the interaction between Brd4 and the E2 protein will be multifactorial. </p></sec><sec><title>4.2. Brd4 Modulates the Stability of the E2 Proteins</title><p>Several groups have noted that the E2 protein is stabilized by interaction with Brd4 [<xref ref-type="bibr" rid="B95-viruses-05-01374">95</xref>,<xref ref-type="bibr" rid="B96-viruses-05-01374">96</xref>] or with the Brd4 CTD [<xref ref-type="bibr" rid="B97-viruses-05-01374">97</xref>]. This interaction prevents proteasomal degradation of E2 by the E3 ligase cullin‑3 [<xref ref-type="bibr" rid="B97-viruses-05-01374">97</xref>] and may enhance many E2 functions, such as transcriptional regulation and stable tethering of genomes on host chromatin. </p></sec><sec><title>4.3. The Role of Brd4 in Viral Transcription</title><p>The E2 protein can both activate or repress viral transcription, depending on whether it binds to sites that are distal or proximal to promoter elements [<xref ref-type="bibr" rid="B5-viruses-05-01374">5</xref>,<xref ref-type="bibr" rid="B8-viruses-05-01374">8</xref>,<xref ref-type="bibr" rid="B9-viruses-05-01374">9</xref>,<xref ref-type="bibr" rid="B10-viruses-05-01374">10</xref>]. Binding of E2 to promoter proximal sites represses the early viral promoter in the oncogenic alpha-PVs [<xref ref-type="bibr" rid="B11-viruses-05-01374">11</xref>,<xref ref-type="bibr" rid="B12-viruses-05-01374">12</xref>,<xref ref-type="bibr" rid="B13-viruses-05-01374">13</xref>]. A number of mutational analyses identified residues in the transactivation domain of E2 that were important for E2‑mediated transcriptional activation or replication [<xref ref-type="bibr" rid="B98-viruses-05-01374">98</xref>,<xref ref-type="bibr" rid="B99-viruses-05-01374">99</xref>,<xref ref-type="bibr" rid="B100-viruses-05-01374">100</xref>,<xref ref-type="bibr" rid="B101-viruses-05-01374">101</xref>,<xref ref-type="bibr" rid="B102-viruses-05-01374">102</xref>,<xref ref-type="bibr" rid="B103-viruses-05-01374">103</xref>]. Prominent were two highly conserved residues (R37 and I73) that when mutated, abrogated E2-mediated transactivation, but not replication. Subsequently, it was shown that these residues were located on two adjacent alpha helices on the same face of the E2 transactivation domain [<xref ref-type="bibr" rid="B104-viruses-05-01374">104</xref>], and later, these residues were shown to make direct contact with a C-terminal peptide (residues 1343–1362) of Brd4 [<xref ref-type="bibr" rid="B91-viruses-05-01374">91</xref>]. In addition to binding to the Brd4 C-terminus, HPV11 E2 also interacts with Brd4 residues 280–580, which encompasses the BD2 bromodomain. </p><p>It became clear that Brd4 was essential for the transcriptional activation function of E2. A dominant negative C-terminal peptide encompassing the Brd4 CTD interfered with the E2-Brd4 interaction and inhibited transactivation by many papillomavirus E2 proteins [<xref ref-type="bibr" rid="B92-viruses-05-01374">92</xref>,<xref ref-type="bibr" rid="B105-viruses-05-01374">105</xref>,<xref ref-type="bibr" rid="B106-viruses-05-01374">106</xref>]. Initially, the role of Brd4 in transcriptional repression was controversial, but it has now been proven that Brd4 is also involved in E2-mediated transcriptional repression [<xref ref-type="bibr" rid="B18-viruses-05-01374">18</xref>,<xref ref-type="bibr" rid="B19-viruses-05-01374">19</xref>,<xref ref-type="bibr" rid="B20-viruses-05-01374">20</xref>]. However, in some cases, the dominant negative Brd4 CTD interferes with E2-mediated transactivation, but not repression, implying that there are additional or alternative modes of interaction between the Brd4 and E2 proteins [<xref ref-type="bibr" rid="B18-viruses-05-01374">18</xref>]. Another factor that contributes to repression of the HPV early promoter is the histone acetyl transferase complex, NuA4/TIP60 [<xref ref-type="bibr" rid="B18-viruses-05-01374">18</xref>,<xref ref-type="bibr" rid="B107-viruses-05-01374">107</xref>]. TIP60 preferentially acetylates K14 of histone H3 and K5, K8, K12 and K16 of histone H4 [<xref ref-type="bibr" rid="B108-viruses-05-01374">108</xref>], which are all targets of the Brd4 bromodomains [<xref ref-type="bibr" rid="B66-viruses-05-01374">66</xref>]. Notably, the HPV E6 protein destabilizes TIP60, thereby alleviating repression of its own promoter [<xref ref-type="bibr" rid="B107-viruses-05-01374">107</xref>]. </p><p>One of the key functions of Brd4 is to recruit p-TEFb to promoters to stimulate elongation of RNA polymerase II transcription. The C-terminal region of Brd4 interacts with both E2 and p-TEFb, suggesting that these complexes are mutually exclusive. Brd4 recruitment of P-TEFb to the early promoter is required for viral transcription, and E2 disrupts this interaction [<xref ref-type="bibr" rid="B109-viruses-05-01374">109</xref>]. In this study (unlike [<xref ref-type="bibr" rid="B18-viruses-05-01374">18</xref>]), the dominant negative BRD4 CTD was able to inhibit E2-mediated repression. </p><p>Most HPV repression studies have analyzed viral transcription in cervical carcinoma-derived cell lines that harbor integrated HPV genomes. However, E2 may preferentially repress integrated genomes compared to episomally replicating genomes, and so, further studies are needed to define the role of Brd4 in HPV transcription [<xref ref-type="bibr" rid="B110-viruses-05-01374">110</xref>].</p></sec><sec><title>4.4. The Role of Brd4 in Viral Genome Replication</title><p>Most studies have indicated that the E2-Brd4 interaction is important for transcriptional regulation and tethering of viral genomes to host chromatin. Mutated E2 proteins that are unable to bind Brd4 are able to efficiently support transient replication of an origin containing plasmid [<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>,<xref ref-type="bibr" rid="B98-viruses-05-01374">98</xref>,<xref ref-type="bibr" rid="B99-viruses-05-01374">99</xref>,<xref ref-type="bibr" rid="B105-viruses-05-01374">105</xref>,<xref ref-type="bibr" rid="B106-viruses-05-01374">106</xref>,<xref ref-type="bibr" rid="B111-viruses-05-01374">111</xref>,<xref ref-type="bibr" rid="B112-viruses-05-01374">112</xref>,<xref ref-type="bibr" rid="B113-viruses-05-01374">113</xref>]. Ilves <italic>et al.</italic> demonstrated that the dominant negative Brd4 CTD could inhibit the replication of BPV1 genomes or origins in rodent cells, but not in human C-33A cells [<xref ref-type="bibr" rid="B113-viruses-05-01374">113</xref>]. Furthermore, this inhibition was not dependent on the interaction of Brd4 with E2 (at least through the R37 and I73 residues) and was not specific for papillomavirus replication [<xref ref-type="bibr" rid="B113-viruses-05-01374">113</xref>]. </p><p>Wang <italic>et al.</italic> find that Brd4 is recruited to foci formed by HPV16 E1 and E2 in a replication origin‑dependent fashion in C-33A cells [<xref ref-type="bibr" rid="B114-viruses-05-01374">114</xref>]. An E2 protein mutated in both Brd4 interacting residues (R37 and I73) is defective in replication, thus leading the authors to propose that Brd4 is required for replication. However, as previously found by others, E2 proteins with a single substitution in I73 are not defective in replication, despite an inability to bind to Brd4 [<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>,<xref ref-type="bibr" rid="B99-viruses-05-01374">99</xref>,<xref ref-type="bibr" rid="B105-viruses-05-01374">105</xref>,<xref ref-type="bibr" rid="B106-viruses-05-01374">106</xref>,<xref ref-type="bibr" rid="B111-viruses-05-01374">111</xref>,<xref ref-type="bibr" rid="B112-viruses-05-01374">112</xref>,<xref ref-type="bibr" rid="B113-viruses-05-01374">113</xref>]. Because downregulation of Brd4 has detrimental effects on cell growth and proliferation (making it difficult to interpret HPV replication experiments), Wang <italic>et al.</italic> demonstrated that Brd4 could stimulate HPV replication <italic>in vitro</italic> [<xref ref-type="bibr" rid="B114-viruses-05-01374">114</xref>].</p><p>Somewhat similarly, we find that Brd4 is recruited to replication foci formed by the E1-E2 proteins in keratinocytes [<xref ref-type="bibr" rid="B49-viruses-05-01374">49</xref>], in a process that is completely dependent on E1, E2 and Brd4. However, we find that Brd4 is displaced to the periphery of these foci in the presence of an actively replicating origin or genome, and Brd4 is no longer required for their formation [<xref ref-type="bibr" rid="B115-viruses-05-01374">115</xref>]. Brd4 is also found in a satellite pattern around late replication foci that contain amplified genomes in differentiated keratinocytes [<xref ref-type="bibr" rid="B115-viruses-05-01374">115</xref>], but it does not seem to be essential for viral DNA amplification [<xref ref-type="bibr" rid="B116-viruses-05-01374">116</xref>]. The HPV replication foci induce a cellular DNA damage response and recruit repair proteins [<xref ref-type="bibr" rid="B46-viruses-05-01374">46</xref>,<xref ref-type="bibr" rid="B47-viruses-05-01374">47</xref>,<xref ref-type="bibr" rid="B48-viruses-05-01374">48</xref>,<xref ref-type="bibr" rid="B49-viruses-05-01374">49</xref>,<xref ref-type="bibr" rid="B50-viruses-05-01374">50</xref>], and it is tempting to speculate that Brd4 is involved in these processes. The replication factor, RF/C, is found in Brd4 [<xref ref-type="bibr" rid="B117-viruses-05-01374">117</xref>] and E2-Brd4 protein complexes [<xref ref-type="bibr" rid="B20-viruses-05-01374">20</xref>,<xref ref-type="bibr" rid="B118-viruses-05-01374">118</xref>]. Furthermore, the alternative RFC1 subunit, ATAD5, which is involved in the DNA damage response, interacts with the ET domain of Brd4 [<xref ref-type="bibr" rid="B71-viruses-05-01374">71</xref>], suggesting that it might play a role in HPV replication. Clearly, more studies are required to elucidate the exact role of Brd4 in the papillomavirus replication process, but there are several hints that Brd4 might be involved in viral and cellular DNA replication and repair processes. </p></sec><sec><title>4.5. The Role of Brd4 in Viral Genome Maintenance and Partitioning</title><p>The E1 and E2 proteins support transient replication, but long-term persistence of viral-derived DNA requires additional E2 binding sites in <italic>cis</italic> to the replication origin [<xref ref-type="bibr" rid="B36-viruses-05-01374">36</xref>]. The first clue to the role of E2 in viral DNA persistence was the observation that both viral DNA and the BPV1 E2 protein are localized in punctate foci on the host mitotic chromosomes [<xref ref-type="bibr" rid="B37-viruses-05-01374">37</xref>]. This led to the model (as shown in <xref ref-type="fig" rid="viruses-05-01374-f004">Figure 4</xref>) that E2 associates with host chromosomes through the transactivation domain [<xref ref-type="bibr" rid="B39-viruses-05-01374">39</xref>], while the DNA binding domain binds to E2 sites in the viral genomes and tethers them to the host chromosomes to promote retention and partitioning [<xref ref-type="bibr" rid="B119-viruses-05-01374">119</xref>]. This tethering mechanism ensures that the low copy viral genome is retained in the nucleus and is partitioned to daughter cells.</p><fig id="viruses-05-01374-f004" position="float"><label>Figure 4</label><caption><p>Model of E2-mediated tethering of the viral genome to host chromatin. The Brd4 protein interacts with acetylated lysine residues on histone tails protruding from the host nucleosomes (shown in purple). The papillomavirus E2 protein interacts with the C‑terminal region of Brd4 through the E2 transactivation domain. The DNA binding‑dimerization domain of E2 links the viral genome to the chromatin complex. </p></caption><graphic xlink:href="viruses-05-01374-g004"></graphic></fig><p>At least for BPV1, the cellular target that mediates mitotic tethering is the Brd4 protein [<xref ref-type="bibr" rid="B72-viruses-05-01374">72</xref>,<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>,<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>]. Brd4 is usually observed as a diffuse cloud (if at all) around the condensed mitotic chromosomes [<xref ref-type="bibr" rid="B59-viruses-05-01374">59</xref>], but in the presence of E2, both proteins colocalize in punctate foci [<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>]. Brd4 has a high on-off rate and can be easily extracted from chromatin [<xref ref-type="bibr" rid="B59-viruses-05-01374">59</xref>], but E2 dramatically stabilizes the interaction of Brd4 with chromatin forming a stable anchor in interphase and mitosis [<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>]. As described above, two highly conserved residues in the transactivation domain of E2 (R37 and I73) mediate the interaction with Brd4, and mutations in these residues abrogate the interaction of E2 with Brd4 and mitotic chromatin [<xref ref-type="bibr" rid="B87-viruses-05-01374">87</xref>]. The DNA binding domain of E2 is not required for the interaction with Brd4, but it is required to link the viral genomes to chromatin [<xref ref-type="bibr" rid="B119-viruses-05-01374">119</xref>]. The dimerization function of the E2 C-terminal domain greatly increases the affinity of Brd4 for chromatin both <italic>in vivo</italic> and <italic>in vitro</italic>, most likely by promoting the assembly of higher order E2-Brd4 complexes [<xref ref-type="bibr" rid="B120-viruses-05-01374">120</xref>]. Expression of the dominant negative Brd4 CTD resulted in inhibition of E2 mitotic chromosome binding and loss of BPV1 genomes from BPV1 transformed cells [<xref ref-type="bibr" rid="B89-viruses-05-01374">89</xref>,<xref ref-type="bibr" rid="B113-viruses-05-01374">113</xref>,<xref ref-type="bibr" rid="B121-viruses-05-01374">121</xref>]. Moreover, BPV1 E2-mediated plasmid maintenance could be reconstituted in <italic>Saccharomyces cerevisiae</italic> by exogenously expressed Brd4 [<xref ref-type="bibr" rid="B122-viruses-05-01374">122</xref>].</p><p>Although the E2 proteins from all papillomaviruses interact with the C-terminal region of Brd4 (through the R37 and I73 residues in E2), there are differences in the strength of binding [<xref ref-type="bibr" rid="B92-viruses-05-01374">92</xref>,<xref ref-type="bibr" rid="B118-viruses-05-01374">118</xref>]. Furthermore, not all E2 proteins are as readily observed bound to mitotic chromosomes as BPV1 E2 [<xref ref-type="bibr" rid="B92-viruses-05-01374">92</xref>,<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>]. A careful analysis of the E2 proteins from numerous different papillomaviruses showed that there were three different phenotypes of mitotic chromosome binding that segregated perfectly according to the phylogeny of papillomaviruses [<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>]. These groups were comprised of the alpha‑papillomaviruses, a large genus that encompasses mainly human viruses that infect the oral and genital mucosa; the beta and gamma papillomaviruses, another large group containing mainly human viruses that infect the cutaneous epithelium in an asymptomatic manner and a diverse group of viruses from the delta (BPV1), mu (HPV1), kappa (OcPV1 and SfPV1) and other genera. The E2 proteins from this latter group bind tightly to Brd4, stabilize its association with interphase chromatin and colocalize with Brd4 on the arms of mitotic chromosomes in punctate dots [<xref ref-type="bibr" rid="B92-viruses-05-01374">92</xref>,<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>].</p><p>In contrast, the beta-PV E2 proteins bind strongly to pericentromeric regions of mitotic chromosomes that overlap the loci for the ribosomal RNA genes [<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>,<xref ref-type="bibr" rid="B124-viruses-05-01374">124</xref>]. The determinants of the E2 protein required for this perichromosomal binding are quite different from those required for the E2‑Brd4 chromosomal foci. The primary requirements are the E2 DNA binding domain and a short peptide from the hinge region that facilitates interaction with chromatin [<xref ref-type="bibr" rid="B125-viruses-05-01374">125</xref>]. Phosphorylation of this peptide by PKA (protein kinase A) stabilizes the E2 protein and promotes chromosomal binding [<xref ref-type="bibr" rid="B126-viruses-05-01374">126</xref>] in a manner analogous to that of the KSHV LANA tethering protein [<xref ref-type="bibr" rid="B127-viruses-05-01374">127</xref>]. However, the beta E2 proteins do have high affinity for Brd4, and if the chromosomal binding peptide in the hinge is mutated, E2-directed foci of Brd4 can be observed on mitotic chromosomes [<xref ref-type="bibr" rid="B128-viruses-05-01374">128</xref>]. The significance of these two binding modes has yet to be determined, as beta-PV genomes do not readily replicate in cell culture.</p><p>For alpha-PVs, the mechanism of E2-mediated viral genome tethering and E2-Brd4 chromosomal binding is still elusive. Alpha-PV E2 proteins bind to Brd4 relatively weakly, they do not stabilize the association of Brd4 with host chromatin and cannot be easily detected on mitotic chromosomes, except in late telophase [<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>,<xref ref-type="bibr" rid="B129-viruses-05-01374">129</xref>]. When cells are pre-extracted before fixation, the alpha-PV E2 proteins bind to the peri-centromeric regions of host chromosomes in a Brd4-independent manner similar to that of the beta-PVs [<xref ref-type="bibr" rid="B123-viruses-05-01374">123</xref>]. Difficulties in detecting alpha-PV E2-Brd4 mitotic foci have led to the proposal of other targets, such as the mitotic spindle [<xref ref-type="bibr" rid="B130-viruses-05-01374">130</xref>], a mitotic kinesin-like protein, MKlp2 [<xref ref-type="bibr" rid="B131-viruses-05-01374">131</xref>], ChlR1 (an ATP-dependent DNA helicase important for sister chromatid cohesion) [<xref ref-type="bibr" rid="B132-viruses-05-01374">132</xref>] and TopBP1 [<xref ref-type="bibr" rid="B129-viruses-05-01374">129</xref>]. Furthermore, HPV31 genomes that encode a Brd4 binding defective E2 protein (an I73L mutation) can still maintain extrachromosomal viral genomes and undergo amplification in differentiated keratinocytes [<xref ref-type="bibr" rid="B54-viruses-05-01374">54</xref>,<xref ref-type="bibr" rid="B105-viruses-05-01374">105</xref>]. Recent findings indicate that Brd4 colocalizes with nuclear foci formed by the alpha-PV E1 and E2 proteins [<xref ref-type="bibr" rid="B114-viruses-05-01374">114</xref>,<xref ref-type="bibr" rid="B115-viruses-05-01374">115</xref>], and we find that the alpha-PV E1-E2 protein complex binds to the same regions of host chromatin as the stable HPV1 E2-Brd4 complex in C-33A cells [<xref ref-type="bibr" rid="B133-viruses-05-01374">133</xref>].</p><p>Therefore, many questions remain, and it seems that the interaction of E2 and Brd4 with host chromatin is complex. The tethering mechanism is likely to be coupled with transcriptional and replication processes. Silla <italic>et al.</italic> have shown that simple attachment of genomes to chromatin is not sufficient [<xref ref-type="bibr" rid="B134-viruses-05-01374">134</xref>]; chromatin attachment and transactivation functions must cooperate to ensure proper plasmid segregation. A genome-wide ChIP-on-chip analysis showed that BPV1 E2 and Brd4 were bound to transcriptionally active regions of chromatin, perhaps to ensure that the viral genome localized to transcriptionally active regions of the nucleus [<xref ref-type="bibr" rid="B135-viruses-05-01374">135</xref>]. Brd4 is recruited to HPV replication centers containing alpha-PV proteins that do not tightly associate with Brd4 [<xref ref-type="bibr" rid="B114-viruses-05-01374">114</xref>,<xref ref-type="bibr" rid="B115-viruses-05-01374">115</xref>]. Thus, transcription, replication and genome partitioning are most likely intertwined processes. </p></sec><sec><title>4.6. Association of Brd4 with Other Viruses</title><p>Papillomaviruses are not the only viruses that have discovered the versatility and usefulness of BET proteins [<xref ref-type="bibr" rid="B136-viruses-05-01374">136</xref>]. The EBNA and LANA tethering proteins of the gamma herpes viruses, EBV and KSHV, interact with Brd2 and Brd4 for transcriptional regulation [<xref ref-type="bibr" rid="B88-viruses-05-01374">88</xref>,<xref ref-type="bibr" rid="B93-viruses-05-01374">93</xref>,<xref ref-type="bibr" rid="B137-viruses-05-01374">137</xref>,<xref ref-type="bibr" rid="B138-viruses-05-01374">138</xref>]. Polyoma viruses also recruit Brd4 to viral replication centers [<xref ref-type="bibr" rid="B139-viruses-05-01374">139</xref>]. Brd4 represses HIV expression by competing with the HIV TAT transactivator for recruitment of p-TEFb to the HIV promoter [<xref ref-type="bibr" rid="B73-viruses-05-01374">73</xref>]. Inhibition of Brd4 with BET inhibitors reactivates latent HIV with great therapeutic potential [<xref ref-type="bibr" rid="B140-viruses-05-01374">140</xref>,<xref ref-type="bibr" rid="B141-viruses-05-01374">141</xref>,<xref ref-type="bibr" rid="B142-viruses-05-01374">142</xref>,<xref ref-type="bibr" rid="B143-viruses-05-01374">143</xref>]. </p></sec></sec><sec><title>5. Conclusions</title><p>Viruses have always alerted us to the key players in cellular processes. Papillomaviruses, in particular, have small genomes with limited coding capacity and rely almost completely on using and manipulating cellular factors for viral processes. Brd4 is clearly a central player in HPV biology, and a complete understanding of its role in essential viral processes will provide deeper insight into its role in host biology.</p></sec></body><back><ack><title>Acknowledgments</title><p>We are grateful to Koenraad van Doorslaer and Wesley Stepp for critical reading of the manuscript. This work was funded by the Intramural Research Program of the NIAID, NIH.</p></ack><notes><title>Conflict of Interest</title><p>The authors declare no conflict of interest.</p></notes><ref-list><title>References and Notes</title><ref id="B1-viruses-05-01374"><label>1.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bouvard</surname><given-names>V.</given-names></name><name><surname>Baan</surname><given-names>R.</given-names></name><name><surname>Straif</surname><given-names>K.</given-names></name><name><surname>Grosse</surname><given-names>Y.</given-names></name><name><surname>Secretan</surname><given-names>B.</given-names></name><name><surname>El</surname><given-names>G.F.</given-names></name><name><surname>Benbrahim-Tallaa</surname><given-names>L.</given-names></name><name><surname>Guha</surname><given-names>N.</given-names></name><name><surname>Freeman</surname><given-names>C.</given-names></name><name><surname>Galichet</surname><given-names>L.</given-names></name><etal></etal></person-group><article-title>A review of human carcinogens—Part B: Biological agents</article-title><source>Lancet Oncol.</source><year>2009</year><volume>10</volume><fpage>321</fpage><lpage>322</lpage><pub-id pub-id-type="doi">10.1016/S1470-2045(09)70096-8</pub-id><pub-id pub-id-type="pmid">19350698</pub-id></element-citation></ref><ref id="B2-viruses-05-01374"><label>2.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Walboomers</surname><given-names>J.M.</given-names></name><name><surname>Jacobs</surname><given-names>M.V.</given-names></name><name><surname>Manos</surname><given-names>M.M.</given-names></name><name><surname>Bosch</surname><given-names>F.X.</given-names></name><name><surname>Kummer</surname><given-names>J.A.</given-names></name><name><surname>Shah</surname><given-names>K.V.</given-names></name><name><surname>Snijders</surname><given-names>P.J.</given-names></name><name><surname>Peto</surname><given-names>J.</given-names></name><name><surname>Meijer</surname><given-names>C.J.</given-names></name><name><surname>Muñoz</surname><given-names>N.</given-names></name></person-group><article-title>Human papillomavirus is a necessary cause of invasive cervical cancer worldwide</article-title><source>J. Pathol.</source><year>1999</year><volume>189</volume><fpage>12</fpage><lpage>19</lpage><pub-id pub-id-type="doi">10.1002/(SICI)1096-9896(199909)189:1<12::AID-PATH431>3.0.CO;2-F</pub-id><pub-id pub-id-type="pmid">10451482</pub-id></element-citation></ref><ref id="B3-viruses-05-01374"><label>3.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gillison</surname><given-names>M.L.</given-names></name><name><surname>Lowy</surname><given-names>D.R.</given-names></name></person-group><article-title>A causal role for human papillomavirus in head and neck cancer</article-title><source>Lancet</source><year>2004</year><volume>363</volume><fpage>1488</fpage><lpage>1489</lpage><pub-id pub-id-type="doi">10.1016/S0140-6736(04)16194-1</pub-id><pub-id pub-id-type="pmid">15135592</pub-id></element-citation></ref><ref id="B4-viruses-05-01374"><label>4.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Johansson</surname><given-names>C.</given-names></name><name><surname>Schwartz</surname><given-names>S.</given-names></name></person-group><article-title>Regulation of human papillomavirus gene expression by splicing and polyadenylation</article-title><source>Nat. Rev. Microbiol.</source><year>2013</year><volume>11</volume><fpage>239</fpage><lpage>251</lpage><pub-id pub-id-type="doi">10.1038/nrmicro2984</pub-id><pub-id pub-id-type="pmid">23474685</pub-id></element-citation></ref><ref id="B5-viruses-05-01374"><label>5.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Spalholz</surname><given-names>B.A.</given-names></name><name><surname>Yang</surname><given-names>Y.C.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Transactivation of a bovine papilloma virus transcriptional regulatory element by the E2 gene product</article-title><source>Cell</source><year>1985</year><volume>42</volume><fpage>183</fpage><lpage>191</lpage><pub-id pub-id-type="doi">10.1016/S0092-8674(85)80114-8</pub-id><pub-id pub-id-type="pmid">2990724</pub-id></element-citation></ref><ref id="B6-viruses-05-01374"><label>6.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>McBride</surname><given-names>A.A.</given-names></name><name><surname>Byrne</surname><given-names>J.C.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>E2 polypeptides encoded by bovine papillomavirus type 1 form dimers through the common carboxyl-terminal domain: Transactivation is mediated by the conserved amino-terminal domain</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>1989</year><volume>86</volume><fpage>510</fpage><lpage>514</lpage><pub-id pub-id-type="doi">10.1073/pnas.86.2.510</pub-id><pub-id pub-id-type="pmid">2536165</pub-id></element-citation></ref><ref id="B7-viruses-05-01374"><label>7.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Androphy</surname><given-names>E.J.</given-names></name><name><surname>Lowy</surname><given-names>D.R.</given-names></name><name><surname>Schiller</surname><given-names>J.T.</given-names></name></person-group><article-title>Bovine papillomavirus E2 trans-activating gene product binds to specific sites in papillomavirus DNA</article-title><source>Nature</source><year>1987</year><volume>325</volume><fpage>70</fpage><lpage>73</lpage><pub-id pub-id-type="doi">10.1038/325070a0</pub-id><pub-id pub-id-type="pmid">3025749</pub-id></element-citation></ref><ref id="B8-viruses-05-01374"><label>8.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cripe</surname><given-names>T.P.</given-names></name><name><surname>Haugen</surname><given-names>T.H.</given-names></name><name><surname>Turk</surname><given-names>J.P.</given-names></name><name><surname>Tabatabai</surname><given-names>F.</given-names></name><name><surname>Schmid</surname><given-names>P.G.</given-names><suffix>3rd.</suffix></name><name><surname>Dürst</surname><given-names>M.</given-names></name><name><surname>Gissmann</surname><given-names>L.</given-names></name><name><surname>Roman</surname><given-names>A.</given-names></name><name><surname>Turek</surname><given-names>L.P.</given-names></name></person-group><article-title>Transcriptional regulation of the human papillomavirus- 16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: Implications for cervical carcinogenesis</article-title><source>EMBO J.</source><year>1987</year><volume>6</volume><fpage>3745</fpage><lpage>3753</lpage><pub-id pub-id-type="pmid">2448139</pub-id></element-citation></ref><ref id="B9-viruses-05-01374"><label>9.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chin</surname><given-names>M.T.</given-names></name><name><surname>Hirochika</surname><given-names>R.</given-names></name><name><surname>Hirochika</surname><given-names>H.</given-names></name><name><surname>Broker</surname><given-names>T.R.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name></person-group><article-title>Regulation of human papillomavirus type 11 enhancer and E6 promoter by activating and repressing proteins from the E2 open reading frame: Functional and biochemical studies</article-title><source>J. Virol.</source><year>1988</year><volume>62</volume><fpage>2994</fpage><lpage>3002</lpage><pub-id pub-id-type="pmid">2839716</pub-id></element-citation></ref><ref id="B10-viruses-05-01374"><label>10.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Steger</surname><given-names>G.</given-names></name><name><surname>Corbach</surname><given-names>S.</given-names></name></person-group><article-title>Dose-dependent regulation of the early promoter of human papillomavirus type 18 by the viral E2 protein</article-title><source>J. Virol.</source><year>1997</year><volume>71</volume><fpage>50</fpage><lpage>58</lpage><pub-id pub-id-type="pmid">8985322</pub-id></element-citation></ref><ref id="B11-viruses-05-01374"><label>11.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Thierry</surname><given-names>F.</given-names></name><name><surname>Yaniv</surname><given-names>M.</given-names></name></person-group><article-title>The BPV1-E2 trans-acting protein can be either an activator or a repressor of the HPV18 regulatory region</article-title><source>EMBO J.</source><year>1987</year><volume>6</volume><fpage>3391</fpage><lpage>3397</lpage><pub-id pub-id-type="pmid">2828029</pub-id></element-citation></ref><ref id="B12-viruses-05-01374"><label>12.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bernard</surname><given-names>B.A.</given-names></name><name><surname>Bailly</surname><given-names>C.</given-names></name><name><surname>Lenoir</surname><given-names>M.C.</given-names></name><name><surname>Darmon</surname><given-names>M.</given-names></name><name><surname>Thierry</surname><given-names>F.</given-names></name><name><surname>Yaniv</surname><given-names>M.</given-names></name></person-group><article-title>The human papillomavirus type 18 (HPV18) E2 gene product is a repressor of the HPV18 regulatory region in human keratinocytes</article-title><source>J. Virol.</source><year>1989</year><volume>63</volume><fpage>4317</fpage><lpage>4324</lpage><pub-id pub-id-type="pmid">2476572</pub-id></element-citation></ref><ref id="B13-viruses-05-01374"><label>13.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Romanczuk</surname><given-names>H.</given-names></name><name><surname>Thierry</surname><given-names>F.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Mutational analysis of cis elements involved in E2 modulation of human papillomavirus type 16 P 97 and type 18 P 105 promoters</article-title><source>J. Virol.</source><year>1990</year><volume>64</volume><fpage>2849</fpage><lpage>2859</lpage><pub-id pub-id-type="pmid">2159546</pub-id></element-citation></ref><ref id="B14-viruses-05-01374"><label>14.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tan</surname><given-names>S.H.</given-names></name><name><surname>Gloss</surname><given-names>B.</given-names></name><name><surname>Bernard</surname><given-names>H.U.</given-names></name></person-group><article-title>During negative regulation of the human papillomavirus-16 E6 promoter, the viral E2 protein can displace Sp1 from a proximal promoter element</article-title><source>Nucleic Acids Res.</source><year>1992</year><volume>20</volume><fpage>251</fpage><lpage>256</lpage><pub-id pub-id-type="doi">10.1093/nar/20.2.251</pub-id><pub-id pub-id-type="pmid">1311070</pub-id></element-citation></ref><ref id="B15-viruses-05-01374"><label>15.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dong</surname><given-names>G.</given-names></name><name><surname>Broker</surname><given-names>T.R.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name></person-group><article-title>Human papillomavirus type 11 E2 proteins repress the homologous E6 promoter by interfering with the binding of host transcription factors to adjacent elements</article-title><source>J. Virol.</source><year>1994</year><volume>68</volume><fpage>1115</fpage><lpage>1127</lpage><pub-id pub-id-type="pmid">8289341</pub-id></element-citation></ref><ref id="B16-viruses-05-01374"><label>16.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tan</surname><given-names>S.H.</given-names></name><name><surname>Leong</surname><given-names>L.E.</given-names></name><name><surname>Walker</surname><given-names>P.A.</given-names></name><name><surname>Bernard</surname><given-names>H.U.</given-names></name></person-group><article-title>The human papillomavirus type 16 E2 transcription factor binds with low cooperativity to two flanking sites and represses the E6 promoter through displacement of Sp1 and TFIID</article-title><source>J. Virol.</source><year>1994</year><volume>68</volume><fpage>6411</fpage><lpage>6420</lpage><pub-id pub-id-type="pmid">8083979</pub-id></element-citation></ref><ref id="B17-viruses-05-01374"><label>17.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nishimura</surname><given-names>A.</given-names></name><name><surname>Ono</surname><given-names>T.</given-names></name><name><surname>Ishimoto</surname><given-names>A.</given-names></name><name><surname>Dowhanick</surname><given-names>J.J.</given-names></name><name><surname>Frizzell</surname><given-names>M.A.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name><name><surname>Sakai</surname><given-names>H.</given-names></name></person-group><article-title>Mechanisms of human papillomavirus E2-mediated repression of viral oncogene expression and cervical cancer cell growth inhibition</article-title><source>J. Virol.</source><year>2000</year><volume>74</volume><fpage>3752</fpage><lpage>3760</lpage><pub-id pub-id-type="doi">10.1128/JVI.74.8.3752-3760.2000</pub-id><pub-id pub-id-type="pmid">10729150</pub-id></element-citation></ref><ref id="B18-viruses-05-01374"><label>18.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Smith</surname><given-names>J.A.</given-names></name><name><surname>White</surname><given-names>E.A.</given-names></name><name><surname>Sowa</surname><given-names>M.E.</given-names></name><name><surname>Powell</surname><given-names>M.L.</given-names></name><name><surname>Ottinger</surname><given-names>M.</given-names></name><name><surname>Harper</surname><given-names>J.W.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Genome-wide siRNA screen identifies SMCX, EP400, and Brd4 as E2-dependent regulators of human papillomavirus oncogene expression</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2010</year><volume>107</volume><fpage>3752</fpage><lpage>3757</lpage><pub-id pub-id-type="pmid">20133580</pub-id></element-citation></ref><ref id="B19-viruses-05-01374"><label>19.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schweiger</surname><given-names>M.R.</given-names></name><name><surname>Ottinger</surname><given-names>M.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Brd4 independent transcriptional repression function of the papillomavirus E2 proteins</article-title><source>J. Virol.</source><year>2007</year><volume>81</volume><fpage>9612</fpage><lpage>9622</lpage><pub-id pub-id-type="doi">10.1128/JVI.00447-07</pub-id><pub-id pub-id-type="pmid">17626100</pub-id></element-citation></ref><ref id="B20-viruses-05-01374"><label>20.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>S.Y.</given-names></name><name><surname>Lee</surname><given-names>A.Y.</given-names></name><name><surname>Hou</surname><given-names>S.Y.</given-names></name><name><surname>Kemper</surname><given-names>J.K.</given-names></name><name><surname>Erdjument-Bromage</surname><given-names>H.</given-names></name><name><surname>Tempst</surname><given-names>P.</given-names></name><name><surname>Chiang</surname><given-names>C.M.</given-names></name></person-group><article-title>Brd4 links chromatin targeting to HPV transcriptional silencing</article-title><source>Genes Dev.</source><year>2006</year><volume>20</volume><fpage>2383</fpage><lpage>2396</lpage><pub-id pub-id-type="doi">10.1101/gad.1448206</pub-id><pub-id pub-id-type="pmid">16921027</pub-id></element-citation></ref><ref id="B21-viruses-05-01374"><label>21.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Thierry</surname><given-names>F.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Functional analysis of E2-mediated repression of the HPV18 P105 promoter</article-title><source>New Biol.</source><year>1991</year><volume>3</volume><fpage>90</fpage><lpage>100</lpage><pub-id pub-id-type="pmid">1645591</pub-id></element-citation></ref><ref id="B22-viruses-05-01374"><label>22.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hwang</surname><given-names>E.S.</given-names></name><name><surname>Riese</surname><given-names>D.J.D.</given-names></name><name><surname>Settleman</surname><given-names>J.</given-names></name><name><surname>Nilson</surname><given-names>L.A.</given-names></name><name><surname>Honig</surname><given-names>J.</given-names></name><name><surname>Flynn</surname><given-names>S.</given-names></name><name><surname>DiMaio</surname><given-names>D.</given-names></name></person-group><article-title>Inhibition of cervical carcinoma cell line proliferation by the introduction of a bovine papillomavirus regulatory gene</article-title><source>J. Virol.</source><year>1993</year><volume>67</volume><fpage>3720</fpage><lpage>3729</lpage><pub-id pub-id-type="pmid">8389903</pub-id></element-citation></ref><ref id="B23-viruses-05-01374"><label>23.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dowhanick</surname><given-names>J.J.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Suppression of cellular proliferation by the papillomavirus E2 protein</article-title><source>J. Virol.</source><year>1995</year><volume>69</volume><fpage>7791</fpage><lpage>7799</lpage><pub-id pub-id-type="pmid">7494290</pub-id></element-citation></ref><ref id="B24-viruses-05-01374"><label>24.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Desaintes</surname><given-names>C.</given-names></name><name><surname>Demeret</surname><given-names>C.</given-names></name><name><surname>Goyat</surname><given-names>S.</given-names></name><name><surname>Yaniv</surname><given-names>M.</given-names></name><name><surname>Thierry</surname><given-names>F.</given-names></name></person-group><article-title>Expression of the papillomavirus E2 protein in HeLa cells leads to apoptosis</article-title><source>EMBO J.</source><year>1997</year><volume>16</volume><fpage>504</fpage><lpage>514</lpage><pub-id pub-id-type="doi">10.1093/emboj/16.3.504</pub-id><pub-id pub-id-type="pmid">9034333</pub-id></element-citation></ref><ref id="B25-viruses-05-01374"><label>25.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stubenrauch</surname><given-names>F.</given-names></name><name><surname>Zobel</surname><given-names>T.</given-names></name><name><surname>Iftner</surname><given-names>T.</given-names></name></person-group><article-title>The E8 domain confers a novel long-distance transcriptional repression activity on the E8E2C protein of high-risk human papillomavirus type 31</article-title><source>J. Virol.</source><year>2001</year><volume>75</volume><fpage>4139</fpage><lpage>4149</lpage><pub-id pub-id-type="doi">10.1128/JVI.75.9.4139-4149.2001</pub-id><pub-id pub-id-type="pmid">11287563</pub-id></element-citation></ref><ref id="B26-viruses-05-01374"><label>26.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chiang</surname><given-names>C.M.</given-names></name><name><surname>Broker</surname><given-names>T.R.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name></person-group><article-title>An E1M^E2C fusion protein encoded by human papillomavirus type 11 is a sequence-specific transcription repressor</article-title><source>J. Virol.</source><year>1991</year><volume>65</volume><fpage>3317</fpage><lpage>3329</lpage><pub-id pub-id-type="pmid">1851879</pub-id></element-citation></ref><ref id="B27-viruses-05-01374"><label>27.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Powell</surname><given-names>M.L.</given-names></name><name><surname>Smith</surname><given-names>J.A.</given-names></name><name><surname>Sowa</surname><given-names>M.E.</given-names></name><name><surname>Harper</surname><given-names>J.W.</given-names></name><name><surname>Iftner</surname><given-names>T.</given-names></name><name><surname>Stubenrauch</surname><given-names>F.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>NCoR1 mediates papillomavirus E8;E2C transcriptional repression</article-title><source>J. Virol.</source><year>2010</year><volume>84</volume><fpage>4451</fpage><lpage>4460</lpage><pub-id pub-id-type="doi">10.1128/JVI.02390-09</pub-id><pub-id pub-id-type="pmid">20181716</pub-id></element-citation></ref><ref id="B28-viruses-05-01374"><label>28.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pett</surname><given-names>M.</given-names></name><name><surname>Coleman</surname><given-names>N.</given-names></name></person-group><article-title>Integration of high-risk human papillomavirus: A key event in cervical carcinogenesis?</article-title><source>J. Pathol.</source><year>2007</year><volume>212</volume><fpage>356</fpage><lpage>367</lpage><pub-id pub-id-type="doi">10.1002/path.2192</pub-id><pub-id pub-id-type="pmid">17573670</pub-id></element-citation></ref><ref id="B29-viruses-05-01374"><label>29.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Francis</surname><given-names>D.A.</given-names></name><name><surname>Schmid</surname><given-names>S.I.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Repression of the integrated papillomavirus E6/E7 promoter is required for growth suppression of cervical cancer cells</article-title><source>J. Virol.</source><year>2000</year><volume>74</volume><fpage>2679</fpage><lpage>2686</lpage><pub-id pub-id-type="doi">10.1128/JVI.74.6.2679-2686.2000</pub-id><pub-id pub-id-type="pmid">10684283</pub-id></element-citation></ref><ref id="B30-viruses-05-01374"><label>30.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jeon</surname><given-names>S.</given-names></name><name><surname>Allen-Hoffmann</surname><given-names>B.L.</given-names></name><name><surname>Lambert</surname><given-names>P.F.</given-names></name></person-group><article-title>Integration of human papillomavirus type 16 into the human genome correlates with a selective growth advantage of cells</article-title><source>J. Virol.</source><year>1995</year><volume>69</volume><fpage>2989</fpage><lpage>2997</lpage><pub-id pub-id-type="pmid">7707525</pub-id></element-citation></ref><ref id="B31-viruses-05-01374"><label>31.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mohr</surname><given-names>I.J.</given-names></name><name><surname>Clark</surname><given-names>R.</given-names></name><name><surname>Sun</surname><given-names>S.</given-names></name><name><surname>Androphy</surname><given-names>E.J.</given-names></name><name><surname>MacPherson</surname><given-names>P.</given-names></name><name><surname>Botchan</surname><given-names>M.R.</given-names></name></person-group><article-title>Targeting the E1 replication protein to the papillomavirus origin of replication by complex formation with the E2 transactivator</article-title><source>Science</source><year>1990</year><volume>250</volume><fpage>1694</fpage><lpage>1699</lpage><pub-id pub-id-type="pmid">2176744</pub-id></element-citation></ref><ref id="B32-viruses-05-01374"><label>32.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ustav</surname><given-names>M.</given-names></name><name><surname>Stenlund</surname><given-names>A.</given-names></name></person-group><article-title>Transient replication of BPV-1 requires two viral polypeptides encoded by the E1 and E2 open reading frames</article-title><source>EMBO J.</source><year>1991</year><volume>10</volume><fpage>449</fpage><lpage>457</lpage><pub-id pub-id-type="pmid">1846806</pub-id></element-citation></ref><ref id="B33-viruses-05-01374"><label>33.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ustav</surname><given-names>M.</given-names></name><name><surname>Ustav</surname><given-names>E.</given-names></name><name><surname>Szymanski</surname><given-names>P.</given-names></name><name><surname>Stenlund</surname><given-names>A.</given-names></name></person-group><article-title>Identification of the origin of replication of bovine papillomavirus and characterization of the viral origin recognition factor E1</article-title><source>EMBO J.</source><year>1991</year><volume>10</volume><fpage>4321</fpage><lpage>4329</lpage><pub-id pub-id-type="pmid">1661672</pub-id></element-citation></ref><ref id="B34-viruses-05-01374"><label>34.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Replication and partitioning of papillomavirus genomes</article-title><source>Adv. Virus Res.</source><year>2008</year><volume>72</volume><fpage>155</fpage><lpage>205</lpage><pub-id pub-id-type="doi">10.1016/S0065-3527(08)00404-1</pub-id><pub-id pub-id-type="pmid">19081491</pub-id></element-citation></ref><ref id="B35-viruses-05-01374"><label>35.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sanders</surname><given-names>C.M.</given-names></name><name><surname>Stenlund</surname><given-names>A.</given-names></name></person-group><article-title>Recruitment and loading of the E1 initiator protein: An ATP-dependent process catalysed by a transcription factor</article-title><source>EMBO J.</source><year>1998</year><volume>17</volume><fpage>7044</fpage><lpage>7055</lpage><pub-id pub-id-type="doi">10.1093/emboj/17.23.7044</pub-id><pub-id pub-id-type="pmid">9843509</pub-id></element-citation></ref><ref id="B36-viruses-05-01374"><label>36.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Piirsoo</surname><given-names>M.</given-names></name><name><surname>Ustav</surname><given-names>E.</given-names></name><name><surname>Mandel</surname><given-names>T.</given-names></name><name><surname>Stenlund</surname><given-names>A.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator</article-title><source>EMBO J.</source><year>1996</year><volume>15</volume><fpage>1</fpage><lpage>11</lpage><pub-id pub-id-type="pmid">8598191</pub-id></element-citation></ref><ref id="B37-viruses-05-01374"><label>37.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Skiadopoulos</surname><given-names>M.H.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Bovine papillomavirus type 1 genomes and the E2 transactivator protein are closely associated with mitotic chromatin</article-title><source>J. Virol.</source><year>1998</year><volume>72</volume><fpage>2079</fpage><lpage>2088</lpage><pub-id pub-id-type="pmid">9499063</pub-id></element-citation></ref><ref id="B38-viruses-05-01374"><label>38.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ilves</surname><given-names>I.</given-names></name><name><surname>Kivi</surname><given-names>S.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Long-term episomal maintenance of bovine papillomavirus type 1 plasmids is determined by attachment to host chromosomes, which is mediated by the viral E2 protein and its binding sites</article-title><source>J. Virol.</source><year>1999</year><volume>73</volume><fpage>4404</fpage><lpage>4412</lpage><pub-id pub-id-type="pmid">10196338</pub-id></element-citation></ref><ref id="B39-viruses-05-01374"><label>39.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bastien</surname><given-names>N.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Interaction of the papillomavirus E2 protein with mitotic chromosomes</article-title><source>Virology</source><year>2000</year><volume>270</volume><fpage>124</fpage><lpage>134</lpage><pub-id pub-id-type="doi">10.1006/viro.2000.0265</pub-id><pub-id pub-id-type="pmid">10772985</pub-id></element-citation></ref><ref id="B40-viruses-05-01374"><label>40.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>K.</given-names></name><name><surname>Lambert</surname><given-names>P.F.</given-names></name></person-group><article-title>E1 protein of bovine papillomavirus 1 is not required for the maintenance of viral plasmid DNA replication</article-title><source>Virology</source><year>2002</year><volume>293</volume><fpage>10</fpage><lpage>14</lpage><pub-id pub-id-type="doi">10.1006/viro.2001.1305</pub-id><pub-id pub-id-type="pmid">11853393</pub-id></element-citation></ref><ref id="B41-viruses-05-01374"><label>41.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Egawa</surname><given-names>N.</given-names></name><name><surname>Nakahara</surname><given-names>T.</given-names></name><name><surname>Ohno</surname><given-names>S.</given-names></name><name><surname>Narisawa-Saito</surname><given-names>M.</given-names></name><name><surname>Yugawa</surname><given-names>T.</given-names></name><name><surname>Fujita</surname><given-names>M.</given-names></name><name><surname>Yamato</surname><given-names>K.</given-names></name><name><surname>Natori</surname><given-names>Y.</given-names></name><name><surname>Kiyono</surname><given-names>T.</given-names></name></person-group><article-title>The E1 protein of human papillomavirus type 16 is dispensable for maintenance replication of the viral genome</article-title><source>J. Virol.</source><year>2012</year><volume>86</volume><fpage>3276</fpage><lpage>3283</lpage><pub-id pub-id-type="doi">10.1128/JVI.06450-11</pub-id><pub-id pub-id-type="pmid">22238312</pub-id></element-citation></ref><ref id="B42-viruses-05-01374"><label>42.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xue</surname><given-names>Y.</given-names></name><name><surname>Bellanger</surname><given-names>S.</given-names></name><name><surname>Zhang</surname><given-names>W.</given-names></name><name><surname>Lim</surname><given-names>D.</given-names></name><name><surname>Low</surname><given-names>J.</given-names></name><name><surname>Lunny</surname><given-names>D.</given-names></name><name><surname>Thierry</surname><given-names>F.</given-names></name></person-group><article-title>HPV16 E2 is an immediate early marker of viral infection, preceding E7 expression in precursor structures of cervical carcinoma</article-title><source>Canc. Res.</source><year>2010</year><volume>70</volume><fpage>5316</fpage><lpage>5325</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-09-3789</pub-id></element-citation></ref><ref id="B43-viruses-05-01374"><label>43.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Penrose</surname><given-names>K.J.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Proteasome-mediated degradation of the papillomavirus E2-TA protein is regulated by phosphorylation and can modulate viral genome copy number</article-title><source>J. Virol.</source><year>2000</year><volume>74</volume><fpage>6031</fpage><lpage>6038</lpage><pub-id pub-id-type="doi">10.1128/JVI.74.13.6031-6038.2000</pub-id><pub-id pub-id-type="pmid">10846085</pub-id></element-citation></ref><ref id="B44-viruses-05-01374"><label>44.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Flores</surname><given-names>E.R.</given-names></name><name><surname>Lambert</surname><given-names>P.F.</given-names></name></person-group><article-title>Evidence for a switch in the mode of human papillomavirus type 16 DNA replication during the viral life cycle</article-title><source>J. Virol.</source><year>1997</year><volume>71</volume><fpage>7167</fpage><lpage>7179</lpage><pub-id pub-id-type="pmid">9311789</pub-id></element-citation></ref><ref id="B45-viruses-05-01374"><label>45.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sakakibara</surname><given-names>N.</given-names></name><name><surname>Chen</surname><given-names>D.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Papillomaviruses use Recombination Dependent Replication to Vegetatively Amplify their Genomes in Differentiated Cells</article-title><source>PLoS Pathog.</source><year>2013</year><comment>in press</comment></element-citation></ref><ref id="B46-viruses-05-01374"><label>46.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gillespie</surname><given-names>K.A.</given-names></name><name><surname>Mehta</surname><given-names>K.P.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name><name><surname>Moody</surname><given-names>C.A.</given-names></name></person-group><article-title>Human papillomaviruses recruit cellular DNA repair and homologous recombination factors to viral replication centers</article-title><source>J. Virol</source><year>2012</year><volume>86</volume><fpage>9520</fpage><lpage>9526</lpage><pub-id pub-id-type="doi">10.1128/JVI.00247-12</pub-id><pub-id pub-id-type="pmid">22740399</pub-id></element-citation></ref><ref id="B47-viruses-05-01374"><label>47.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moody</surname><given-names>C.A.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name></person-group><article-title>Human papillomaviruses activate the ATM DNA damage pathway for viral genome amplification upon differentiation</article-title><source>PLoS Pathog.</source><year>2009</year><volume>5</volume><fpage>e1000605</fpage><pub-id pub-id-type="doi">10.1371/journal.ppat.1000605</pub-id><pub-id pub-id-type="pmid">19798429</pub-id></element-citation></ref><ref id="B48-viruses-05-01374"><label>48.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fradet-Turcotte</surname><given-names>A.</given-names></name><name><surname>Bergeron-Labrecque</surname><given-names>F.</given-names></name><name><surname>Moody</surname><given-names>C.A.</given-names></name><name><surname>Lehoux</surname><given-names>M.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name><name><surname>Archambault</surname><given-names>J.</given-names></name></person-group><article-title>Nuclear accumulation of the papillomavirus E1 helicase blocks S-phase progression and triggers an ATM-dependent DNA damage response</article-title><source>J. Virol.</source><year>2011</year><volume>85</volume><fpage>8996</fpage><lpage>9012</lpage><pub-id pub-id-type="doi">10.1128/JVI.00542-11</pub-id><pub-id pub-id-type="pmid">21734051</pub-id></element-citation></ref><ref id="B49-viruses-05-01374"><label>49.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sakakibara</surname><given-names>N.</given-names></name><name><surname>Mitra</surname><given-names>R.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>The papillomavirus E1 helicase activates a cellular DNA damage response in viral replication foci</article-title><source>J. Virol.</source><year>2011</year><volume>85</volume><fpage>8981</fpage><lpage>8995</lpage><pub-id pub-id-type="doi">10.1128/JVI.00541-11</pub-id><pub-id pub-id-type="pmid">21734054</pub-id></element-citation></ref><ref id="B50-viruses-05-01374"><label>50.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Reinson</surname><given-names>T.</given-names></name><name><surname>Toots</surname><given-names>M.</given-names></name><name><surname>Kadaja</surname><given-names>M.</given-names></name><name><surname>Pipitch</surname><given-names>R.</given-names></name><name><surname>Allik</surname><given-names>M.</given-names></name><name><surname>Ustav</surname><given-names>E.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Engagement of the ATR-dependent DNA damage response at the human papillomavirus 18 replication centers during the initial amplification</article-title><source>J. Virol.</source><year>2013</year><volume>87</volume><fpage>951</fpage><lpage>964</lpage><pub-id pub-id-type="doi">10.1128/JVI.01943-12</pub-id><pub-id pub-id-type="pmid">23135710</pub-id></element-citation></ref><ref id="B51-viruses-05-01374"><label>51.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Swindle</surname><given-names>C.S.</given-names></name><name><surname>Zou</surname><given-names>N.</given-names></name><name><surname>Van Tine</surname><given-names>B.A.</given-names></name><name><surname>Shaw</surname><given-names>G.M.</given-names></name><name><surname>Engler</surname><given-names>J.A.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name></person-group><article-title>Human papillomavirus DNA replication compartments in a transient DNA replication system</article-title><source>J. Virol.</source><year>1999</year><volume>73</volume><fpage>1001</fpage><lpage>1009</lpage><pub-id pub-id-type="pmid">9882301</pub-id></element-citation></ref><ref id="B52-viruses-05-01374"><label>52.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Van Doorslaer</surname><given-names>K.</given-names></name><name><surname>Tan</surname><given-names>Q.</given-names></name><name><surname>Xirasagar</surname><given-names>S.</given-names></name><name><surname>Bandaru</surname><given-names>S.</given-names></name><name><surname>Gopalan</surname><given-names>V.</given-names></name><name><surname>Mohamoud</surname><given-names>Y.</given-names></name><name><surname>Huyen</surname><given-names>Y.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>The Papillomavirus Episteme: A central resource for papillomavirus sequence data and analysis</article-title><source>Nucleic Acids Res.</source><year>2013</year><volume>41</volume><fpage>D571</fpage><lpage>D578</lpage><pub-id pub-id-type="doi">10.1093/nar/gks984</pub-id><pub-id pub-id-type="pmid">23093593</pub-id></element-citation></ref><ref id="B53-viruses-05-01374"><label>53.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>R.</given-names></name><name><surname>Knight</surname><given-names>J.</given-names></name><name><surname>Bream</surname><given-names>G.</given-names></name><name><surname>Stenlund</surname><given-names>A.</given-names></name><name><surname>Botchan</surname><given-names>M.</given-names></name></person-group><article-title>Specific recognition nucleotides and their DNA context determine the affinity of E2 protein for 17 binding sites in the BPV-1 genome</article-title><source>Genes Dev.</source><year>1989</year><volume>3</volume><fpage>510</fpage><lpage>526</lpage><pub-id pub-id-type="doi">10.1101/gad.3.4.510</pub-id><pub-id pub-id-type="pmid">2542129</pub-id></element-citation></ref><ref id="B54-viruses-05-01374"><label>54.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stubenrauch</surname><given-names>F.</given-names></name><name><surname>Lim</surname><given-names>H.B.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name></person-group><article-title>Differential requirements for conserved E2 binding sites in the life cycle of oncogenic human papillomavirus type 31</article-title><source>J. Virol.</source><year>1998</year><volume>72</volume><fpage>1071</fpage><lpage>1077</lpage><pub-id pub-id-type="pmid">9445001</pub-id></element-citation></ref><ref id="B55-viruses-05-01374"><label>55.</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Van Doorslaer</surname><given-names>K.</given-names></name><name><surname>Khan</surname><given-names>J.</given-names></name><name><surname>Chapman</surname><given-names>S.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Three E2 binding sites are sufficient for stable episomal maintenance of HPV18</article-title><publisher-name>National Institutes of Health</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc><year>2013</year><comment>To be submitted for publication</comment></element-citation></ref><ref id="B56-viruses-05-01374"><label>56.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dey</surname><given-names>A.</given-names></name><name><surname>Ellenberg</surname><given-names>J.</given-names></name><name><surname>Farina</surname><given-names>A.</given-names></name><name><surname>Coleman</surname><given-names>A.E.</given-names></name><name><surname>Maruyama</surname><given-names>T.</given-names></name><name><surname>Sciortino</surname><given-names>S.</given-names></name><name><surname>Lippincott-Schwartz</surname><given-names>J.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>A bromodomain protein, MCAP, associates with mitotic chromosomes and affects G(2)-to-M transition</article-title><source>Mol. Cell Biol.</source><year>2000</year><volume>20</volume><fpage>6537</fpage><lpage>6549</lpage><pub-id pub-id-type="doi">10.1128/MCB.20.17.6537-6549.2000</pub-id><pub-id pub-id-type="pmid">10938129</pub-id></element-citation></ref><ref id="B57-viruses-05-01374"><label>57.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Florence</surname><given-names>B.</given-names></name><name><surname>Faller</surname><given-names>D.V.</given-names></name></person-group><article-title>You bet-cha: A novel family of transcriptional regulators</article-title><source>Front. Biosci.</source><year>2001</year><volume>6</volume><fpage>D1008</fpage><lpage>D1018</lpage><pub-id pub-id-type="doi">10.2741/Florence</pub-id><pub-id pub-id-type="pmid">11487468</pub-id></element-citation></ref><ref id="B58-viruses-05-01374"><label>58.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Houzelstein</surname><given-names>D.</given-names></name><name><surname>Bullock</surname><given-names>S.L.</given-names></name><name><surname>Lynch</surname><given-names>D.E.</given-names></name><name><surname>Grigorieva</surname><given-names>E.F.</given-names></name><name><surname>Wilson</surname><given-names>V.A.</given-names></name><name><surname>Beddington</surname><given-names>R.S.</given-names></name></person-group><article-title>Growth and early postimplantation defects in mice deficient for the bromodomain-containing protein Brd4</article-title><source>Mol. Cell Biol.</source><year>2002</year><volume>22</volume><fpage>3794</fpage><lpage>3802</lpage><pub-id pub-id-type="doi">10.1128/MCB.22.11.3794-3802.2002</pub-id><pub-id pub-id-type="pmid">11997514</pub-id></element-citation></ref><ref id="B59-viruses-05-01374"><label>59.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dey</surname><given-names>A.</given-names></name><name><surname>Chitsaz</surname><given-names>F.</given-names></name><name><surname>Abbasi</surname><given-names>A.</given-names></name><name><surname>Misteli</surname><given-names>T.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>The double bromodomain protein Brd4 binds to acetylated chromatin during interphase and mitosis</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2003</year><volume>100</volume><fpage>8758</fpage><lpage>8763</lpage><pub-id pub-id-type="doi">10.1073/pnas.1433065100</pub-id><pub-id pub-id-type="pmid">12840145</pub-id></element-citation></ref><ref id="B60-viruses-05-01374"><label>60.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dey</surname><given-names>A.</given-names></name><name><surname>Nishiyama</surname><given-names>A.</given-names></name><name><surname>Karpova</surname><given-names>T.</given-names></name><name><surname>McNally</surname><given-names>J.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>Brd4 marks select genes on mitotic chromatin and directs postmitotic transcription</article-title><source>Mol. Biol. Cell</source><year>2009</year><volume>20</volume><fpage>4899</fpage><lpage>4909</lpage><pub-id pub-id-type="doi">10.1091/mbc.E09-05-0380</pub-id><pub-id pub-id-type="pmid">19812244</pub-id></element-citation></ref><ref id="B61-viruses-05-01374"><label>61.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mochizuki</surname><given-names>K.</given-names></name><name><surname>Nishiyama</surname><given-names>A.</given-names></name><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Dey</surname><given-names>A.</given-names></name><name><surname>Ghosh</surname><given-names>A.</given-names></name><name><surname>Tamura</surname><given-names>T.</given-names></name><name><surname>Natsume</surname><given-names>H.</given-names></name><name><surname>Yao</surname><given-names>H.J.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>The bromodomain protein Brd4 stimulates G(1) gene transcription and promotes progression to S phase</article-title><source>J. Biol. Chem.</source><year>2008</year><volume>283</volume><fpage>9040</fpage><lpage>9048</lpage><pub-id pub-id-type="doi">10.1074/jbc.M707603200</pub-id><pub-id pub-id-type="pmid">18223296</pub-id></element-citation></ref><ref id="B62-viruses-05-01374"><label>62.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>R.</given-names></name><name><surname>Nakamura</surname><given-names>T.</given-names></name><name><surname>Fu</surname><given-names>Y.</given-names></name><name><surname>Lazar</surname><given-names>Z.</given-names></name><name><surname>Spector</surname><given-names>D.L.</given-names></name></person-group><article-title>Gene bookmarking accelerates the kinetics of post-mitotic transcriptional re-activation</article-title><source>Nat. Cell Biol.</source><year>2011</year><volume>13</volume><fpage>1295</fpage><lpage>1304</lpage><pub-id pub-id-type="doi">10.1038/ncb2341</pub-id><pub-id pub-id-type="pmid">21983563</pub-id></element-citation></ref><ref id="B63-viruses-05-01374"><label>63.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Mochizuki</surname><given-names>K.</given-names></name><name><surname>Zhou</surname><given-names>M.</given-names></name><name><surname>Jeong</surname><given-names>H.S.</given-names></name><name><surname>Brady</surname><given-names>J.N.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription</article-title><source>Mol. Cell</source><year>2005</year><volume>19</volume><fpage>523</fpage><lpage>534</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2005.06.027</pub-id><pub-id pub-id-type="pmid">16109376</pub-id></element-citation></ref><ref id="B64-viruses-05-01374"><label>64.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>Z.</given-names></name><name><surname>Yik</surname><given-names>J.H.</given-names></name><name><surname>Chen</surname><given-names>R.</given-names></name><name><surname>He</surname><given-names>N.</given-names></name><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>Zhou</surname><given-names>Q.</given-names></name></person-group><article-title>Recruitment of P-TEFb for stimulation of transcriptional elongation by the bromodomain protein Brd4</article-title><source>Mol. Cell</source><year>2005</year><volume>19</volume><fpage>535</fpage><lpage>545</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2005.06.029</pub-id><pub-id pub-id-type="pmid">16109377</pub-id></element-citation></ref><ref id="B65-viruses-05-01374"><label>65.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Devaiah</surname><given-names>B.N.</given-names></name><name><surname>Singer</surname><given-names>D.S.</given-names></name></person-group><article-title>Two faces of brd4: Mitotic bookmark and transcriptional lynchpin</article-title><source>Transcription</source><year>2013</year><volume>4</volume><fpage>13</fpage><lpage>17</lpage><pub-id pub-id-type="doi">10.4161/trns.22542</pub-id><pub-id pub-id-type="pmid">23131666</pub-id></element-citation></ref><ref id="B66-viruses-05-01374"><label>66.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Filippakopoulos</surname><given-names>P.</given-names></name><name><surname>Picaud</surname><given-names>S.</given-names></name><name><surname>Mangos</surname><given-names>M.</given-names></name><name><surname>Keates</surname><given-names>T.</given-names></name><name><surname>Lambert</surname><given-names>J.P.</given-names></name><name><surname>Barsyte-Lovejoy</surname><given-names>D.</given-names></name><name><surname>Felletar</surname><given-names>I.</given-names></name><name><surname>Volkmer</surname><given-names>R.</given-names></name><name><surname>Muller</surname><given-names>S.</given-names></name><name><surname>Pawson</surname><given-names>T.</given-names></name><etal></etal></person-group><article-title>Histone recognition and large-scale structural analysis of the human bromodomain family</article-title><source>Cell</source><year>2012</year><volume>149</volume><fpage>214</fpage><lpage>231</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2012.02.013</pub-id><pub-id pub-id-type="pmid">22464331</pub-id></element-citation></ref><ref id="B67-viruses-05-01374"><label>67.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vollmuth</surname><given-names>F.</given-names></name><name><surname>Blankenfeldt</surname><given-names>W.</given-names></name><name><surname>Geyer</surname><given-names>M.</given-names></name></person-group><article-title>Structures of the dual bromodomains of the P-TEFb-activating protein Brd4 at atomic resolution</article-title><source>J. Biol. Chem.</source><year>2009</year><volume>284</volume><fpage>36547</fpage><lpage>36556</lpage><pub-id pub-id-type="doi">10.1074/jbc.M109.033712</pub-id><pub-id pub-id-type="pmid">19828451</pub-id></element-citation></ref><ref id="B68-viruses-05-01374"><label>68.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schröder</surname><given-names>S.</given-names></name><name><surname>Cho</surname><given-names>S.</given-names></name><name><surname>Zeng</surname><given-names>L.</given-names></name><name><surname>Zhang</surname><given-names>Q.</given-names></name><name><surname>Kaehlcke</surname><given-names>K.</given-names></name><name><surname>Mak</surname><given-names>L.</given-names></name><name><surname>Lau</surname><given-names>J.</given-names></name><name><surname>Bisgrove</surname><given-names>D.</given-names></name><name><surname>Schnölzer</surname><given-names>M.</given-names></name><name><surname>Verdin</surname><given-names>E.</given-names></name></person-group><article-title>Two-pronged binding with bromodomain-containing protein 4 liberates positive transcription elongation factor b from inactive ribonucleoprotein complexes</article-title><source>J. Biol. Chem.</source><year>2012</year><volume>287</volume><fpage>1090</fpage><lpage>1099</lpage><pub-id pub-id-type="doi">10.1074/jbc.M111.282855</pub-id><pub-id pub-id-type="pmid">22084242</pub-id></element-citation></ref><ref id="B69-viruses-05-01374"><label>69.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>B.</given-names></name><name><surname>Yang</surname><given-names>X.D.</given-names></name><name><surname>Zhou</surname><given-names>M.M.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>Chen</surname><given-names>L.F.</given-names></name></person-group><article-title>Brd4 coactivates transcriptional activation of NF-kappaB via specific binding to acetylated RelA</article-title><source>Mol. Cell Biol.</source><year>2009</year><volume>29</volume><fpage>1375</fpage><lpage>1387</lpage><pub-id pub-id-type="doi">10.1128/MCB.01365-08</pub-id><pub-id pub-id-type="pmid">19103749</pub-id></element-citation></ref><ref id="B70-viruses-05-01374"><label>70.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lin</surname><given-names>Y.J.</given-names></name><name><surname>Umehara</surname><given-names>T.</given-names></name><name><surname>Inoue</surname><given-names>M.</given-names></name><name><surname>Saito</surname><given-names>K.</given-names></name><name><surname>Kigawa</surname><given-names>T.</given-names></name><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>Yokoyama</surname><given-names>S.</given-names></name><name><surname>Padmanabhan</surname><given-names>B.</given-names></name><name><surname>Guntert</surname><given-names>P.</given-names></name></person-group><article-title>Solution structure of the extraterminal domain of the bromodomain-containing protein BRD4</article-title><source>Protein Sci.</source><year>2008</year><volume>17</volume><fpage>2174</fpage><lpage>2179</lpage><pub-id pub-id-type="doi">10.1110/ps.037580.108</pub-id><pub-id pub-id-type="pmid">18815416</pub-id></element-citation></ref><ref id="B71-viruses-05-01374"><label>71.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rahman</surname><given-names>S.</given-names></name><name><surname>Sowa</surname><given-names>M.E.</given-names></name><name><surname>Ottinger</surname><given-names>M.</given-names></name><name><surname>Smith</surname><given-names>J.A.</given-names></name><name><surname>Shi</surname><given-names>Y.</given-names></name><name><surname>Harper</surname><given-names>J.W.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>The Brd4 extraterminal domain confers transcription activation independent of pTEFb by recruiting multiple proteins, including NSD3</article-title><source>Mol. Cell Biol.</source><year>2011</year><volume>31</volume><fpage>2641</fpage><lpage>2652</lpage><pub-id pub-id-type="doi">10.1128/MCB.01341-10</pub-id><pub-id pub-id-type="pmid">21555454</pub-id></element-citation></ref><ref id="B72-viruses-05-01374"><label>72.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>You</surname><given-names>J.</given-names></name><name><surname>Croyle</surname><given-names>J.L.</given-names></name><name><surname>Nishimura</surname><given-names>A.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Interaction of the bovine papillomavirus E2 protein with Brd4 tethers the viral DNA to host mitotic chromosomes</article-title><source>Cell</source><year>2004</year><volume>117</volume><fpage>349</fpage><lpage>360</lpage><pub-id pub-id-type="doi">10.1016/S0092-8674(04)00402-7</pub-id><pub-id pub-id-type="pmid">15109495</pub-id></element-citation></ref><ref id="B73-viruses-05-01374"><label>73.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bisgrove</surname><given-names>D.A.</given-names></name><name><surname>Mahmoudi</surname><given-names>T.</given-names></name><name><surname>Henklein</surname><given-names>P.</given-names></name><name><surname>Verdin</surname><given-names>E.</given-names></name></person-group><article-title>Conserved P-TEFb-interacting domain of BRD4 inhibits HIV transcription</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2007</year><volume>104</volume><fpage>13690</fpage><lpage>13695</lpage><pub-id pub-id-type="pmid">17690245</pub-id></element-citation></ref><ref id="B74-viruses-05-01374"><label>74.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>S.Y.</given-names></name><name><surname>Lee</surname><given-names>A.Y.</given-names></name><name><surname>Lai</surname><given-names>H.T.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Chiang</surname><given-names>C.M.</given-names></name></person-group><article-title>Phospho switch triggers brd4 chromatin binding and activator recruitment for gene-specific targeting</article-title><source>Mol. Cell</source><year>2013</year><volume>49</volume><fpage>843</fpage><lpage>857</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2012.12.006</pub-id><pub-id pub-id-type="pmid">23317504</pub-id></element-citation></ref><ref id="B75-viruses-05-01374"><label>75.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>French</surname><given-names>C.A.</given-names></name><name><surname>Miyoshi</surname><given-names>I.</given-names></name><name><surname>Aster</surname><given-names>J.C.</given-names></name><name><surname>Kubonishi</surname><given-names>I.</given-names></name><name><surname>Kroll</surname><given-names>T.G.</given-names></name><name><surname>Dal Cin</surname><given-names>P.</given-names></name><name><surname>Vargas</surname><given-names>S.O.</given-names></name><name><surname>Perez-Atayde</surname><given-names>A.R.</given-names></name><name><surname>Fletcher</surname><given-names>J.A.</given-names></name></person-group><article-title>BRD4 bromodomain gene rearrangement in aggressive carcinoma with translocation t(15;19)</article-title><source>Am. J. Pathol.</source><year>2001</year><volume>159</volume><fpage>1987</fpage><lpage>1992</lpage><pub-id pub-id-type="doi">10.1016/S0002-9440(10)63049-0</pub-id><pub-id pub-id-type="pmid">11733348</pub-id></element-citation></ref><ref id="B76-viruses-05-01374"><label>76.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Reynoird</surname><given-names>N.</given-names></name><name><surname>Schwartz</surname><given-names>B.E.</given-names></name><name><surname>Delvecchio</surname><given-names>M.</given-names></name><name><surname>Sadoul</surname><given-names>K.</given-names></name><name><surname>Meyers</surname><given-names>D.</given-names></name><name><surname>Mukherjee</surname><given-names>C.</given-names></name><name><surname>Caron</surname><given-names>C.</given-names></name><name><surname>Kimura</surname><given-names>H.</given-names></name><name><surname>Rousseaux</surname><given-names>S.</given-names></name><name><surname>Cole</surname><given-names>P.A.</given-names></name><etal></etal></person-group><article-title>Oncogenesis by sequestration of CBP/p300 in transcriptionally inactive hyperacetylated chromatin domains</article-title><source>EMBO J.</source><year>2010</year><volume>29</volume><fpage>2943</fpage><lpage>2952</lpage><pub-id pub-id-type="doi">10.1038/emboj.2010.176</pub-id><pub-id pub-id-type="pmid">20676058</pub-id></element-citation></ref><ref id="B77-viruses-05-01374"><label>77.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Filippakopoulos</surname><given-names>P.</given-names></name><name><surname>Qi</surname><given-names>J.</given-names></name><name><surname>Picaud</surname><given-names>S.</given-names></name><name><surname>Shen</surname><given-names>Y.</given-names></name><name><surname>Smith</surname><given-names>W.B.</given-names></name><name><surname>Fedorov</surname><given-names>O.</given-names></name><name><surname>Morse</surname><given-names>E.M.</given-names></name><name><surname>Keates</surname><given-names>T.</given-names></name><name><surname>Hickman</surname><given-names>T.T.</given-names></name><name><surname>Felletar</surname><given-names>I.</given-names></name><etal></etal></person-group><article-title>Selective inhibition of BET bromodomains</article-title><source>Nature</source><year>2010</year><volume>468</volume><fpage>1067</fpage><lpage>1073</lpage><pub-id pub-id-type="doi">10.1038/nature09504</pub-id><pub-id pub-id-type="pmid">20871596</pub-id></element-citation></ref><ref id="B78-viruses-05-01374"><label>78.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schwartz</surname><given-names>B.E.</given-names></name><name><surname>Hofer</surname><given-names>M.D.</given-names></name><name><surname>Lemieux</surname><given-names>M.E.</given-names></name><name><surname>Bauer</surname><given-names>D.E.</given-names></name><name><surname>Cameron</surname><given-names>M.J.</given-names></name><name><surname>West</surname><given-names>N.H.</given-names></name><name><surname>Agoston</surname><given-names>E.S.</given-names></name><name><surname>Reynoird</surname><given-names>N.</given-names></name><name><surname>Khochbin</surname><given-names>S.</given-names></name><name><surname>Ince</surname><given-names>T.A.</given-names></name><etal></etal></person-group><article-title>Differentiation of NUT midline carcinoma by epigenomic reprogramming</article-title><source>Canc. Res.</source><year>2011</year><volume>71</volume><fpage>2686</fpage><lpage>2696</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-10-3513</pub-id></element-citation></ref><ref id="B79-viruses-05-01374"><label>79.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yan</surname><given-names>J.</given-names></name><name><surname>Diaz</surname><given-names>J.</given-names></name><name><surname>Jiao</surname><given-names>J.</given-names></name><name><surname>Wang</surname><given-names>R.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name></person-group><article-title>Perturbation of BRD4 protein function by BRD4-NUT protein abrogates cellular differentiation in NUT midline carcinoma</article-title><source>J. Biol. Chem.</source><year>2011</year><volume>286</volume><fpage>27663</fpage><lpage>27675</lpage><pub-id pub-id-type="doi">10.1074/jbc.M111.246975</pub-id><pub-id pub-id-type="pmid">21652721</pub-id></element-citation></ref><ref id="B80-viruses-05-01374"><label>80.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Crawford</surname><given-names>N.P.S.</given-names></name><name><surname>Alsarraj</surname><given-names>J.</given-names></name><name><surname>Lukes</surname><given-names>L.</given-names></name><name><surname>Walker</surname><given-names>R.C.</given-names></name><name><surname>Officewala</surname><given-names>J.S.</given-names></name><name><surname>Yang</surname><given-names>H.H.</given-names></name><name><surname>Lee</surname><given-names>M.P.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>Hunter</surname><given-names>K.W.</given-names></name></person-group><article-title>Bromodomain 4 activation predicts breast cancer survival</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2008</year><volume>105</volume><fpage>6380</fpage><lpage>6385</lpage><pub-id pub-id-type="doi">10.1073/pnas.0710331105</pub-id><pub-id pub-id-type="pmid">18427120</pub-id></element-citation></ref><ref id="B81-viruses-05-01374"><label>81.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lockwood</surname><given-names>W.W.</given-names></name><name><surname>Zejnullahu</surname><given-names>K.</given-names></name><name><surname>Bradner</surname><given-names>J.E.</given-names></name><name><surname>Varmus</surname><given-names>H.</given-names></name></person-group><article-title>Sensitivity of human lung adenocarcinoma cell lines to targeted inhibition of BET epigenetic signaling proteins</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2012</year><volume>109</volume><fpage>19408</fpage><lpage>19413</lpage><pub-id pub-id-type="pmid">23129625</pub-id></element-citation></ref><ref id="B82-viruses-05-01374"><label>82.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ott</surname><given-names>C.J.</given-names></name><name><surname>Kopp</surname><given-names>N.</given-names></name><name><surname>Bird</surname><given-names>L.</given-names></name><name><surname>Paranal</surname><given-names>R.M.</given-names></name><name><surname>Qi</surname><given-names>J.</given-names></name><name><surname>Bowman</surname><given-names>T.</given-names></name><name><surname>Rodig</surname><given-names>S.J.</given-names></name><name><surname>Kung</surname><given-names>A.L.</given-names></name><name><surname>Bradner</surname><given-names>J.E.</given-names></name><name><surname>Weinstock</surname><given-names>D.M.</given-names></name></person-group><article-title>BET bromodomain inhibition targets both c-Myc and IL7R in high-risk acute lymphoblastic leukemia</article-title><source>Blood</source><year>2012</year><volume>120</volume><fpage>2843</fpage><lpage>2852</lpage><pub-id pub-id-type="doi">10.1182/blood-2012-02-413021</pub-id><pub-id pub-id-type="pmid">22904298</pub-id></element-citation></ref><ref id="B83-viruses-05-01374"><label>83.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dawson</surname><given-names>M.A.</given-names></name><name><surname>Prinjha</surname><given-names>R.K.</given-names></name><name><surname>Dittmann</surname><given-names>A.</given-names></name><name><surname>Giotopoulos</surname><given-names>G.</given-names></name><name><surname>Bantscheff</surname><given-names>M.</given-names></name><name><surname>Chan</surname><given-names>W.I.</given-names></name><name><surname>Robson</surname><given-names>S.C.</given-names></name><name><surname>Chung</surname><given-names>C.W.</given-names></name><name><surname>Hopf</surname><given-names>C.</given-names></name><name><surname>Savitski</surname><given-names>M.M.</given-names></name><etal></etal></person-group><article-title>Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia</article-title><source>Nature</source><year>2011</year><volume>478</volume><fpage>529</fpage><lpage>533</lpage><pub-id pub-id-type="doi">10.1038/nature10509</pub-id><pub-id pub-id-type="pmid">21964340</pub-id></element-citation></ref><ref id="B84-viruses-05-01374"><label>84.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Delmore</surname><given-names>J.E.</given-names></name><name><surname>Issa</surname><given-names>G.C.</given-names></name><name><surname>Lemieux</surname><given-names>M.E.</given-names></name><name><surname>Rahl</surname><given-names>P.B.</given-names></name><name><surname>Shi</surname><given-names>J.</given-names></name><name><surname>Jacobs</surname><given-names>H.M.</given-names></name><name><surname>Kastritis</surname><given-names>E.</given-names></name><name><surname>Gilpatrick</surname><given-names>T.</given-names></name><name><surname>Paranal</surname><given-names>R.M.</given-names></name><name><surname>Qi</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>BET bromodomain inhibition as a therapeutic strategy to target c-Myc</article-title><source>Cell</source><year>2011</year><volume>146</volume><fpage>904</fpage><lpage>917</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2011.08.017</pub-id><pub-id pub-id-type="pmid">21889194</pub-id></element-citation></ref><ref id="B85-viruses-05-01374"><label>85.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mertz</surname><given-names>J.A.</given-names></name><name><surname>Conery</surname><given-names>A.R.</given-names></name><name><surname>Bryant</surname><given-names>B.M.</given-names></name><name><surname>Sandy</surname><given-names>P.</given-names></name><name><surname>Balasubramanian</surname><given-names>S.</given-names></name><name><surname>Mele</surname><given-names>D.A.</given-names></name><name><surname>Bergeron</surname><given-names>L.</given-names></name><name><surname>Sims</surname><given-names>R.J.</given-names><suffix>3rd.</suffix></name></person-group><article-title>Targeting MYC dependence in cancer by inhibiting BET bromodomains</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2011</year><volume>108</volume><fpage>16669</fpage><lpage>16674</lpage><pub-id pub-id-type="doi">10.1073/pnas.1108190108</pub-id><pub-id pub-id-type="pmid">21949397</pub-id></element-citation></ref><ref id="B86-viruses-05-01374"><label>86.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Olejnik-Schmidt</surname><given-names>A.K.</given-names></name><name><surname>Schmidt</surname><given-names>M.T.</given-names></name><name><surname>Kedzia</surname><given-names>W.</given-names></name><name><surname>Gozdzicka-Jozefiak</surname><given-names>A.</given-names></name></person-group><article-title>Search for cellular partners of human papillomavirus type 16 E2 protein</article-title><source>Arch. Virol.</source><year>2008</year><volume>153</volume><fpage>983</fpage><lpage>990</lpage><pub-id pub-id-type="doi">10.1007/s00705-008-0061-6</pub-id><pub-id pub-id-type="pmid">18305892</pub-id></element-citation></ref><ref id="B87-viruses-05-01374"><label>87.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Baxter</surname><given-names>M.K.</given-names></name><name><surname>McPhillips</surname><given-names>M.G.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>The mitotic chromosome binding activity of the papillomavirus E2 protein correlates with interaction with the cellular chromosomal protein, Brd4</article-title><source>J. Virol.</source><year>2005</year><volume>79</volume><fpage>4806</fpage><lpage>4818</lpage><pub-id pub-id-type="doi">10.1128/JVI.79.8.4806-4818.2005</pub-id><pub-id pub-id-type="pmid">15795266</pub-id></element-citation></ref><ref id="B88-viruses-05-01374"><label>88.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Platt</surname><given-names>G.M.</given-names></name><name><surname>Simpson</surname><given-names>G.R.</given-names></name><name><surname>Mittnacht</surname><given-names>S.</given-names></name><name><surname>Schulz</surname><given-names>T.F.</given-names></name></person-group><article-title>Latent nuclear antigen of Kaposi's sarcoma-associated herpesvirus interacts with RING3, a homolog of the Drosophila female sterile homeotic (fsh) gene</article-title><source>J. Virol.</source><year>1999</year><volume>73</volume><fpage>9789</fpage><lpage>9795</lpage><pub-id pub-id-type="pmid">10559289</pub-id></element-citation></ref><ref id="B89-viruses-05-01374"><label>89.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>McPhillips</surname><given-names>M.G.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Interaction of bovine papillomavirus E2 protein with Brd4 stabilizes its association with chromatin</article-title><source>J. Virol.</source><year>2005</year><volume>79</volume><fpage>8920</fpage><lpage>8932</lpage><pub-id pub-id-type="doi">10.1128/JVI.79.14.8920-8932.2005</pub-id><pub-id pub-id-type="pmid">15994786</pub-id></element-citation></ref><ref id="B90-viruses-05-01374"><label>90.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lehman</surname><given-names>C.W.</given-names></name><name><surname>Botchan</surname><given-names>M.R.</given-names></name></person-group><article-title>Segregation of viral plasmids depends on tethering to chromosomes and is regulated by phosphorylation</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>1998</year><volume>95</volume><fpage>4338</fpage><lpage>4343</lpage><pub-id pub-id-type="doi">10.1073/pnas.95.8.4338</pub-id><pub-id pub-id-type="pmid">9539738</pub-id></element-citation></ref><ref id="B91-viruses-05-01374"><label>91.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Abbate</surname><given-names>E.A.</given-names></name><name><surname>Voitenleitner</surname><given-names>C.</given-names></name><name><surname>Botchan</surname><given-names>M.R.</given-names></name></person-group><article-title>Structure of the papillomavirus DNA-tethering complex E2:Brd4 and a peptide that ablates HPV chromosomal association</article-title><source>Mol. Cell</source><year>2006</year><volume>24</volume><fpage>877</fpage><lpage>889</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2006.11.002</pub-id><pub-id pub-id-type="pmid">17189190</pub-id></element-citation></ref><ref id="B92-viruses-05-01374"><label>92.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>McPhillips</surname><given-names>M.G.</given-names></name><name><surname>Oliveira</surname><given-names>J.G.</given-names></name><name><surname>Spindler</surname><given-names>J.E.</given-names></name><name><surname>Mitra</surname><given-names>R.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Brd4 is required for e2-mediated transcriptional activation but not genome partitioning of all papillomaviruses</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>9530</fpage><lpage>9543</lpage><pub-id pub-id-type="doi">10.1128/JVI.01105-06</pub-id><pub-id pub-id-type="pmid">16973557</pub-id></element-citation></ref><ref id="B93-viruses-05-01374"><label>93.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ottinger</surname><given-names>M.</given-names></name><name><surname>Christalla</surname><given-names>T.</given-names></name><name><surname>Nathan</surname><given-names>K.</given-names></name><name><surname>Brinkmann</surname><given-names>M.M.</given-names></name><name><surname>Viejo-Borbolla</surname><given-names>A.</given-names></name><name><surname>Schulz</surname><given-names>T.F.</given-names></name></person-group><article-title>The Kaposi’s Sarcoma-Associated Herpesvirus LANA-1 interacts with the short variant of BRD4 and releases cells from a BRD4- and BRD2/RING3-induced G1 cell cycle arrest</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>10772</fpage><lpage>10786</lpage><pub-id pub-id-type="doi">10.1128/JVI.00804-06</pub-id><pub-id pub-id-type="pmid">16928766</pub-id></element-citation></ref><ref id="B94-viruses-05-01374"><label>94.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>You</surname><given-names>J.</given-names></name><name><surname>Srinivasan</surname><given-names>V.</given-names></name><name><surname>Denis</surname><given-names>G.V.</given-names></name><name><surname>Harrington</surname><given-names>W.J.</given-names><suffix>Jr.</suffix></name><name><surname>Ballestas</surname><given-names>M.E.</given-names></name><name><surname>Kaye</surname><given-names>K.M.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Kaposi’s sarcoma-associated herpesvirus latency-associated nuclear antigen interacts with bromodomain protein Brd4 on host mitotic chromosomes</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>8909</fpage><lpage>8919</lpage><pub-id pub-id-type="doi">10.1128/JVI.00502-06</pub-id><pub-id pub-id-type="pmid">16940503</pub-id></element-citation></ref><ref id="B95-viruses-05-01374"><label>95.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>A.Y.</given-names></name><name><surname>Chiang</surname><given-names>C.M.</given-names></name></person-group><article-title>Chromatin adaptor Brd4 modulates E2 transcription activity and protein stability</article-title><source>J. Biol. Chem.</source><year>2009</year><volume>284</volume><fpage>2778</fpage><lpage>2786</lpage><pub-id pub-id-type="pmid">19038968</pub-id></element-citation></ref><ref id="B96-viruses-05-01374"><label>96.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gagnon</surname><given-names>D.</given-names></name><name><surname>Joubert</surname><given-names>S.</given-names></name><name><surname>Senechal</surname><given-names>H.</given-names></name><name><surname>Fradet-Turcotte</surname><given-names>A.</given-names></name><name><surname>Torre</surname><given-names>S.</given-names></name><name><surname>Archambault</surname><given-names>J.</given-names></name></person-group><article-title>Proteasomal degradation of the papillomavirus E2 protein is inhibited by overexpression of bromodomain-containing protein 4</article-title><source>J. Virol.</source><year>2009</year><volume>83</volume><fpage>4127</fpage><lpage>4139</lpage><pub-id pub-id-type="doi">10.1128/JVI.02468-08</pub-id><pub-id pub-id-type="pmid">19211738</pub-id></element-citation></ref><ref id="B97-viruses-05-01374"><label>97.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zheng</surname><given-names>G.</given-names></name><name><surname>Schweiger</surname><given-names>M.R.</given-names></name><name><surname>Martinez-Noel</surname><given-names>G.</given-names></name><name><surname>Zheng</surname><given-names>L.</given-names></name><name><surname>Smith</surname><given-names>J.A.</given-names></name><name><surname>Harper</surname><given-names>J.W.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Brd4 regulation of papillomavirus protein E2 stability</article-title><source>J. Virol.</source><year>2009</year><volume>83</volume><fpage>8683</fpage><lpage>8692</lpage><pub-id pub-id-type="doi">10.1128/JVI.00674-09</pub-id><pub-id pub-id-type="pmid">19553317</pub-id></element-citation></ref><ref id="B98-viruses-05-01374"><label>98.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Winokur</surname><given-names>P.L.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Separation of the transcriptional activation and replication functions of the bovine papillomavirus-1 E2 protein</article-title><source>EMBO J.</source><year>1992</year><volume>11</volume><fpage>4111</fpage><lpage>4118</lpage><pub-id pub-id-type="pmid">1327758</pub-id></element-citation></ref><ref id="B99-viruses-05-01374"><label>99.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sakai</surname><given-names>H.</given-names></name><name><surname>Yasugi</surname><given-names>T.</given-names></name><name><surname>Benson</surname><given-names>J.D.</given-names></name><name><surname>Dowhanick</surname><given-names>J.J.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Targeted mutagenesis of the human papillomavirus type 16 E2 transactivation domain reveals separable transcriptional activation and DNA replication functions</article-title><source>J. Virol.</source><year>1996</year><volume>70</volume><fpage>1602</fpage><lpage>1611</lpage><pub-id pub-id-type="pmid">8627680</pub-id></element-citation></ref><ref id="B100-viruses-05-01374"><label>100.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Abroi</surname><given-names>A.</given-names></name><name><surname>Kurg</surname><given-names>R.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Transcriptional and replicational activation functions in the BPV1 E2 protein are encoded by different structural determinants</article-title><source>J. Virol.</source><year>1996</year><volume>70</volume><fpage>6169</fpage><lpage>6179</lpage><pub-id pub-id-type="pmid">8709243</pub-id></element-citation></ref><ref id="B101-viruses-05-01374"><label>101.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Breiding</surname><given-names>D.E.</given-names></name><name><surname>Grossel</surname><given-names>M.J.</given-names></name><name><surname>Androphy</surname><given-names>E.J.</given-names></name></person-group><article-title>Genetic analysis of the bovine papillomavirus E2 transcriptional activation domain</article-title><source>Virology</source><year>1996</year><volume>221</volume><fpage>34</fpage><lpage>43</lpage><pub-id pub-id-type="doi">10.1006/viro.1996.0350</pub-id><pub-id pub-id-type="pmid">8661412</pub-id></element-citation></ref><ref id="B102-viruses-05-01374"><label>102.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ferguson</surname><given-names>M.F.</given-names></name><name><surname>Botchan</surname><given-names>M.R.</given-names></name></person-group><article-title>Genetic analysis of the activation domain of bovine papillomavirus protein E2:its role in transcription and replication</article-title><source>J. Virol.</source><year>1996</year><volume>70</volume><fpage>4193</fpage><lpage>4199</lpage><pub-id pub-id-type="pmid">8676438</pub-id></element-citation></ref><ref id="B103-viruses-05-01374"><label>103.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cooper</surname><given-names>C.S.</given-names></name><name><surname>Upmeyer</surname><given-names>S.N.</given-names></name><name><surname>Winokur</surname><given-names>P.L.</given-names></name></person-group><article-title>Identification of single amino acids in the human papillomavirus 11 E2 protein critical for the transactivation or replication functions</article-title><source>Virology</source><year>1998</year><volume>241</volume><fpage>312</fpage><lpage>322</lpage><pub-id pub-id-type="doi">10.1006/viro.1997.8941</pub-id><pub-id pub-id-type="pmid">9499806</pub-id></element-citation></ref><ref id="B104-viruses-05-01374"><label>104.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Antson</surname><given-names>A.A.</given-names></name><name><surname>Burns</surname><given-names>J.E.</given-names></name><name><surname>Moroz</surname><given-names>O.V.</given-names></name><name><surname>Scott</surname><given-names>D.J.</given-names></name><name><surname>Sanders</surname><given-names>C.M.</given-names></name><name><surname>Bronstein</surname><given-names>I.B.</given-names></name><name><surname>Dodson</surname><given-names>G.G.</given-names></name><name><surname>Wilson</surname><given-names>K.S.</given-names></name><name><surname>Maitland</surname><given-names>N.J.</given-names></name></person-group><article-title>Structure of the intact transactivation domain of the human papillomavirus E2 protein</article-title><source>Nature</source><year>2000</year><volume>403</volume><fpage>805</fpage><lpage>809</lpage><pub-id pub-id-type="doi">10.1038/35001638</pub-id><pub-id pub-id-type="pmid">10693813</pub-id></element-citation></ref><ref id="B105-viruses-05-01374"><label>105.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Senechal</surname><given-names>H.</given-names></name><name><surname>Poirier</surname><given-names>G.G.</given-names></name><name><surname>Coulombe</surname><given-names>B.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name><name><surname>Archambault</surname><given-names>J.</given-names></name></person-group><article-title>Amino acid substitutions that specifically impair the transcriptional activity of papillomavirus E2 affect binding to the long isoform of Brd4</article-title><source>Virology</source><year>2007</year><volume>358</volume><fpage>10</fpage><lpage>17</lpage><pub-id pub-id-type="doi">10.1016/j.virol.2006.08.035</pub-id><pub-id pub-id-type="pmid">17023018</pub-id></element-citation></ref><ref id="B106-viruses-05-01374"><label>106.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schweiger</surname><given-names>M.R.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Bromodomain protein 4 mediates the papillomavirus e2 transcriptional activation function</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>4276</fpage><lpage>4285</lpage><pub-id pub-id-type="doi">10.1128/JVI.80.9.4276-4285.2006</pub-id><pub-id pub-id-type="pmid">16611886</pub-id></element-citation></ref><ref id="B107-viruses-05-01374"><label>107.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jha</surname><given-names>S.</given-names></name><name><surname>Vande</surname><given-names>P.S.</given-names></name><name><surname>Banerjee</surname><given-names>N.S.</given-names></name><name><surname>Dutta</surname><given-names>A.B.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name><name><surname>Dutta</surname><given-names>A.</given-names></name></person-group><article-title>Destabilization of TIP60 by human papillomavirus E6 results in attenuation of TIP60-dependent transcriptional regulation and apoptotic pathway</article-title><source>Mol. Cell</source><year>2010</year><volume>38</volume><fpage>700</fpage><lpage>711</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2010.05.020</pub-id><pub-id pub-id-type="pmid">20542002</pub-id></element-citation></ref><ref id="B108-viruses-05-01374"><label>108.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kimura</surname><given-names>A.</given-names></name><name><surname>Horikoshi</surname><given-names>M.</given-names></name></person-group><article-title>Tip60 acetylates six lysines of a specific class in core histones <italic>in vitro</italic></article-title><source>Gene. Cell.</source><year>1998</year><volume>3</volume><fpage>789</fpage><lpage>800</lpage><pub-id pub-id-type="doi">10.1046/j.1365-2443.1998.00229.x</pub-id></element-citation></ref><ref id="B109-viruses-05-01374"><label>109.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yan</surname><given-names>J.</given-names></name><name><surname>Li</surname><given-names>Q.</given-names></name><name><surname>Lievens</surname><given-names>S.</given-names></name><name><surname>Tavernier</surname><given-names>J.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name></person-group><article-title>Abrogation of the Brd4-positive transcription elongation factor B complex by papillomavirus E2 protein contributes to viral oncogene repression</article-title><source>J. Virol.</source><year>2010</year><volume>84</volume><fpage>76</fpage><lpage>87</lpage><pub-id pub-id-type="doi">10.1128/JVI.01647-09</pub-id><pub-id pub-id-type="pmid">19846528</pub-id></element-citation></ref><ref id="B110-viruses-05-01374"><label>110.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bechtold</surname><given-names>V.</given-names></name><name><surname>Beard</surname><given-names>P.</given-names></name><name><surname>Raj</surname><given-names>K.</given-names></name></person-group><article-title>Human papillomavirus type 16 E2 protein has no effect on transcription from episomal viral DNA</article-title><source>J. Virol.</source><year>2003</year><volume>77</volume><fpage>2021</fpage><lpage>2028</lpage><pub-id pub-id-type="doi">10.1128/JVI.77.3.2021-2028.2003</pub-id><pub-id pub-id-type="pmid">12525636</pub-id></element-citation></ref><ref id="B111-viruses-05-01374"><label>111.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Baxter</surname><given-names>M.K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>An acidic amphipathic helix in the Bovine Papillomavirus E2 protein is critical for DNA replication and interaction with the E1 protein</article-title><source>Virology</source><year>2005</year><volume>332</volume><fpage>78</fpage><lpage>88</lpage><pub-id pub-id-type="doi">10.1016/j.virol.2004.11.036</pub-id><pub-id pub-id-type="pmid">15661142</pub-id></element-citation></ref><ref id="B112-viruses-05-01374"><label>112.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Brokaw</surname><given-names>J.L.</given-names></name><name><surname>Blanco</surname><given-names>M.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Amino acids critical for the functions of the bovine papillomavirus type 1 E2 transactivator</article-title><source>J. Virol.</source><year>1996</year><volume>70</volume><fpage>23</fpage><lpage>29</lpage><pub-id pub-id-type="pmid">8523530</pub-id></element-citation></ref><ref id="B113-viruses-05-01374"><label>113.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ilves</surname><given-names>I.</given-names></name><name><surname>Maemets</surname><given-names>K.</given-names></name><name><surname>Silla</surname><given-names>T.</given-names></name><name><surname>Janikson</surname><given-names>K.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Brd4 is involved in multiple processes of the bovine papillomavirus type 1 life cycle</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>3660</fpage><lpage>3665</lpage><pub-id pub-id-type="doi">10.1128/JVI.80.7.3660-3665.2006</pub-id><pub-id pub-id-type="pmid">16537635</pub-id></element-citation></ref><ref id="B114-viruses-05-01374"><label>114.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Helfer</surname><given-names>C.M.</given-names></name><name><surname>Pancholi</surname><given-names>N.</given-names></name><name><surname>Bradner</surname><given-names>J.E.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name></person-group><article-title>Recruitment of brd4 to the human papillomavirus type 16 DNA replication complex is essential for replication of viral DNA</article-title><source>J. Virol.</source><year>2013</year><volume>87</volume><fpage>3871</fpage><lpage>3884</lpage><pub-id pub-id-type="doi">10.1128/JVI.03068-12</pub-id><pub-id pub-id-type="pmid">23365439</pub-id></element-citation></ref><ref id="B115-viruses-05-01374"><label>115.</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Sakakibara</surname><given-names>N.</given-names></name><name><surname>Chen</surname><given-names>D.</given-names></name><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>The Brd4 Chromatin Adaptor Protein is displaced from nuclear foci as the HPV E2 protein switches from Transcriptional to Replicational Modes</article-title><publisher-name>National Institutes of Health</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc><year>2013</year><comment>Submitted for publication</comment></element-citation></ref><ref id="B116-viruses-05-01374"><label>116.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stubenrauch</surname><given-names>F.</given-names></name><name><surname>Colbert</surname><given-names>A.M.</given-names></name><name><surname>Laimins</surname><given-names>L.A.</given-names></name></person-group><article-title>Transactivation by the E2 protein of oncogenic human papillomavirus type 31 is not essential for early and late viral functions</article-title><source>J. Virol.</source><year>1998</year><volume>72</volume><fpage>8115</fpage><lpage>8123</lpage><pub-id pub-id-type="pmid">9733852</pub-id></element-citation></ref><ref id="B117-viruses-05-01374"><label>117.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Maruyama</surname><given-names>T.</given-names></name><name><surname>Farina</surname><given-names>A.</given-names></name><name><surname>Dey</surname><given-names>A.</given-names></name><name><surname>Cheong</surname><given-names>J.</given-names></name><name><surname>Bermudez</surname><given-names>V.P.</given-names></name><name><surname>Tamura</surname><given-names>T.</given-names></name><name><surname>Sciortino</surname><given-names>S.</given-names></name><name><surname>Shuman</surname><given-names>J.</given-names></name><name><surname>Hurwitz</surname><given-names>J.</given-names></name><name><surname>Ozato</surname><given-names>K.</given-names></name></person-group><article-title>A Mammalian bromodomain protein, Brd4, interacts with replication factor C and inhibits progression to S phase</article-title><source>Mol. Cell Biol.</source><year>2002</year><volume>22</volume><fpage>6509</fpage><lpage>6520</lpage><pub-id pub-id-type="doi">10.1128/MCB.22.18.6509-6520.2002</pub-id><pub-id pub-id-type="pmid">12192049</pub-id></element-citation></ref><ref id="B118-viruses-05-01374"><label>118.</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><publisher-name>National Institutes of Health</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc><year>2013</year><comment>Unpublished work</comment></element-citation></ref><ref id="B119-viruses-05-01374"><label>119.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Abroi</surname><given-names>A.</given-names></name><name><surname>Ilves</surname><given-names>I.</given-names></name><name><surname>Kivi</surname><given-names>S.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Analysis of chromatin attachment and partitioning functions of bovine papillomavirus type 1 E2 protein</article-title><source>J. Virol.</source><year>2004</year><volume>78</volume><fpage>2100</fpage><lpage>2113</lpage><pub-id pub-id-type="doi">10.1128/JVI.78.4.2100-2113.2004</pub-id><pub-id pub-id-type="pmid">14747575</pub-id></element-citation></ref><ref id="B120-viruses-05-01374"><label>120.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cardenas-Mora</surname><given-names>J.</given-names></name><name><surname>Spindler</surname><given-names>J.E.</given-names></name><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Dimerization of the papillomavirus E2 protein is required for efficient mitotic chromosome association and Brd4 binding</article-title><source>J. Virol.</source><year>2008</year><volume>82</volume><fpage>7298</fpage><lpage>7305</lpage><pub-id pub-id-type="doi">10.1128/JVI.00772-08</pub-id><pub-id pub-id-type="pmid">18495759</pub-id></element-citation></ref><ref id="B121-viruses-05-01374"><label>121.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>You</surname><given-names>J.</given-names></name><name><surname>Schweiger</surname><given-names>M.R.</given-names></name><name><surname>Howley</surname><given-names>P.M.</given-names></name></person-group><article-title>Inhibition of E2 binding to Brd4 enhances viral genome loss and phenotypic reversion of bovine papillomavirus-transformed cells</article-title><source>J. Virol.</source><year>2005</year><volume>79</volume><fpage>14956</fpage><lpage>14961</lpage><pub-id pub-id-type="doi">10.1128/JVI.79.23.14956-14961.2005</pub-id><pub-id pub-id-type="pmid">16282494</pub-id></element-citation></ref><ref id="B122-viruses-05-01374"><label>122.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Brannon</surname><given-names>A.R.</given-names></name><name><surname>Maresca</surname><given-names>J.A.</given-names></name><name><surname>Boeke</surname><given-names>J.D.</given-names></name><name><surname>Basrai</surname><given-names>M.A.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Reconstitution of papillomavirus E2-mediated plasmid maintenance in Saccharomyces cerevisiae by the Brd4 bromodomain protein</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2005</year><volume>102</volume><fpage>2998</fpage><lpage>3003</lpage><pub-id pub-id-type="doi">10.1073/pnas.0407818102</pub-id><pub-id pub-id-type="pmid">15710895</pub-id></element-citation></ref><ref id="B123-viruses-05-01374"><label>123.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Oliveira</surname><given-names>J.G.</given-names></name><name><surname>Colf</surname><given-names>L.A.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Variations in the association of papillomavirus E2 proteins with mitotic chromosomes</article-title><source>Proc. Natl. Acad. Sci. USA</source><year>2006</year><volume>103</volume><fpage>1047</fpage><lpage>1052</lpage><pub-id pub-id-type="doi">10.1073/pnas.0507624103</pub-id><pub-id pub-id-type="pmid">16415162</pub-id></element-citation></ref><ref id="B124-viruses-05-01374"><label>124.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Poddar</surname><given-names>A.</given-names></name><name><surname>Reed</surname><given-names>S.C.</given-names></name><name><surname>McPhillips</surname><given-names>M.G.</given-names></name><name><surname>Spindler</surname><given-names>J.E.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>The human papillomavirus type 8 E2 tethering protein targets the ribosomal DNA loci of host mitotic chromosomes</article-title><source>J. Virol.</source><year>2009</year><volume>83</volume><fpage>640</fpage><lpage>650</lpage><pub-id pub-id-type="doi">10.1128/JVI.01936-08</pub-id><pub-id pub-id-type="pmid">19004936</pub-id></element-citation></ref><ref id="B125-viruses-05-01374"><label>125.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sekhar</surname><given-names>V.</given-names></name><name><surname>Reed</surname><given-names>S.C.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Interaction of the betapapillomavirus E2 tethering protein with mitotic chromosomes</article-title><source>J. Virol.</source><year>2010</year><volume>84</volume><fpage>543</fpage><lpage>557</lpage><pub-id pub-id-type="doi">10.1128/JVI.01908-09</pub-id><pub-id pub-id-type="pmid">19846509</pub-id></element-citation></ref><ref id="B126-viruses-05-01374"><label>126.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sekhar</surname><given-names>V.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Phosphorylation regulates binding of the human papillomavirus type 8 E2 protein to host chromosomes</article-title><source>J. Virol.</source><year>2012</year><volume>86</volume><fpage>10047</fpage><lpage>10058</lpage><pub-id pub-id-type="doi">10.1128/JVI.01140-12</pub-id><pub-id pub-id-type="pmid">22787207</pub-id></element-citation></ref><ref id="B127-viruses-05-01374"><label>127.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Woodard</surname><given-names>C.</given-names></name><name><surname>Shamay</surname><given-names>M.</given-names></name><name><surname>Liao</surname><given-names>G.</given-names></name><name><surname>Zhu</surname><given-names>J.</given-names></name><name><surname>Ng</surname><given-names>A.N.</given-names></name><name><surname>Li</surname><given-names>R.</given-names></name><name><surname>Newman</surname><given-names>R.</given-names></name><name><surname>Rho</surname><given-names>H.S.</given-names></name><name><surname>Hu</surname><given-names>J.</given-names></name><name><surname>Wan</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>Phosphorylation of the chromatin binding domain of KSHV LANA</article-title><source>PLoS Pathog.</source><year>2012</year><volume>8</volume><fpage>e1002972</fpage><pub-id pub-id-type="doi">10.1371/journal.ppat.1002972</pub-id><pub-id pub-id-type="pmid">23093938</pub-id></element-citation></ref><ref id="B128-viruses-05-01374"><label>128.</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>McBride</surname><given-names>A.A.</given-names></name><name><surname>van Doorslaer</surname><given-names>K.</given-names></name></person-group><publisher-name>National Institutes of Health</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc><year>2013</year><comment>Unpublished work</comment></element-citation></ref><ref id="B129-viruses-05-01374"><label>129.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Donaldson</surname><given-names>M.M.</given-names></name><name><surname>Boner</surname><given-names>W.</given-names></name><name><surname>Morgan</surname><given-names>I.M.</given-names></name></person-group><article-title>TopBP1 regulates human papillomavirus type 16 E2 interaction with chromatin</article-title><source>J. Virol.</source><year>2007</year><volume>81</volume><fpage>4338</fpage><lpage>4342</lpage><pub-id pub-id-type="doi">10.1128/JVI.02353-06</pub-id><pub-id pub-id-type="pmid">17287259</pub-id></element-citation></ref><ref id="B130-viruses-05-01374"><label>130.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dao</surname><given-names>L.D.</given-names></name><name><surname>Duffy</surname><given-names>A.</given-names></name><name><surname>van Tine</surname><given-names>B.A.</given-names></name><name><surname>Wu</surname><given-names>S.Y.</given-names></name><name><surname>Chiang</surname><given-names>C.M.</given-names></name><name><surname>Broker</surname><given-names>T.R.</given-names></name><name><surname>Chow</surname><given-names>L.T.</given-names></name></person-group><article-title>Dynamic localization of the human papillomavirus type 11 origin binding protein E2 through mitosis while in association with the spindle apparatus</article-title><source>J. Virol.</source><year>2006</year><volume>80</volume><fpage>4792</fpage><lpage>4800</lpage><pub-id pub-id-type="doi">10.1128/JVI.80.10.4792-4800.2006</pub-id><pub-id pub-id-type="pmid">16641272</pub-id></element-citation></ref><ref id="B131-viruses-05-01374"><label>131.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yu</surname><given-names>T.</given-names></name><name><surname>Peng</surname><given-names>Y.C.</given-names></name><name><surname>Androphy</surname><given-names>E.J.</given-names></name></person-group><article-title>Mitotic kinesin-like protein 2 binds and colocalizes with papillomavirus E2 during mitosis</article-title><source>J. Virol.</source><year>2007</year><volume>81</volume><fpage>1736</fpage><lpage>1745</lpage><pub-id pub-id-type="doi">10.1128/JVI.01638-06</pub-id><pub-id pub-id-type="pmid">17135315</pub-id></element-citation></ref><ref id="B132-viruses-05-01374"><label>132.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Parish</surname><given-names>J.L.</given-names></name><name><surname>Bean</surname><given-names>A.M.</given-names></name><name><surname>Park</surname><given-names>R.B.</given-names></name><name><surname>Androphy</surname><given-names>E.J.</given-names></name></person-group><article-title>ChlR1 is required for loading papillomavirus E2 onto mitotic chromosomes and viral genome maintenance</article-title><source>Mol. Cell</source><year>2006</year><volume>24</volume><fpage>867</fpage><lpage>876</lpage><pub-id pub-id-type="doi">10.1016/j.molcel.2006.11.005</pub-id><pub-id pub-id-type="pmid">17189189</pub-id></element-citation></ref><ref id="B133-viruses-05-01374"><label>133.</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Sakakibara</surname><given-names>N.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Papillomavirus Genomes associate with the Cellular Protein Brd4 to replicate at Fragile Sites in the Host Genome</article-title><publisher-name>National Institutes of Health</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc><year>2013</year><comment>Submitted for publication</comment></element-citation></ref><ref id="B134-viruses-05-01374"><label>134.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Silla</surname><given-names>T.</given-names></name><name><surname>Mannik</surname><given-names>A.</given-names></name><name><surname>Ustav</surname><given-names>M.</given-names></name></person-group><article-title>Effective formation of the segregation-competent complex determines successful partitioning of the bovine papillomavirus genome during cell division</article-title><source>J. Virol.</source><year>2010</year><volume>84</volume><fpage>11175</fpage><lpage>11188</lpage><pub-id pub-id-type="doi">10.1128/JVI.01366-10</pub-id><pub-id pub-id-type="pmid">20810736</pub-id></element-citation></ref><ref id="B135-viruses-05-01374"><label>135.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jang</surname><given-names>M.K.</given-names></name><name><surname>Kwon</surname><given-names>D.</given-names></name><name><surname>McBride</surname><given-names>A.A.</given-names></name></person-group><article-title>Papillomavirus E2 proteins and the host BRD4 protein associate with transcriptionally active cellular chromatin</article-title><source>J. Virol.</source><year>2009</year><volume>83</volume><fpage>2592</fpage><lpage>2600</lpage><pub-id pub-id-type="doi">10.1128/JVI.02275-08</pub-id><pub-id pub-id-type="pmid">19129460</pub-id></element-citation></ref><ref id="B136-viruses-05-01374"><label>136.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Weidner-Glunde</surname><given-names>M.</given-names></name><name><surname>Ottinger</surname><given-names>M.</given-names></name><name><surname>Schulz</surname><given-names>T.F.</given-names></name></person-group><article-title>WHAT do viruses BET on?</article-title><source>Front. Biosci.</source><year>2010</year><volume>15</volume><fpage>537</fpage><lpage>549</lpage><pub-id pub-id-type="doi">10.2741/3632</pub-id><pub-id pub-id-type="pmid">20036832</pub-id></element-citation></ref><ref id="B137-viruses-05-01374"><label>137.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lin</surname><given-names>A.</given-names></name><name><surname>Wang</surname><given-names>S.</given-names></name><name><surname>Nguyen</surname><given-names>T.</given-names></name><name><surname>Shire</surname><given-names>K.</given-names></name><name><surname>Frappier</surname><given-names>L.</given-names></name></person-group><article-title>The EBNA1 protein of Epstein-Barr virus functionally interacts with Brd4</article-title><source>J. Virol.</source><year>2008</year><volume>82</volume><fpage>12009</fpage><lpage>12019</lpage><pub-id pub-id-type="doi">10.1128/JVI.01680-08</pub-id><pub-id pub-id-type="pmid">18922874</pub-id></element-citation></ref><ref id="B138-viruses-05-01374"><label>138.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Viejo-Borbolla</surname><given-names>A.</given-names></name><name><surname>Kati</surname><given-names>E.</given-names></name><name><surname>Sheldon</surname><given-names>J.A.</given-names></name><name><surname>Nathan</surname><given-names>K.</given-names></name><name><surname>Mattsson</surname><given-names>K.</given-names></name><name><surname>Szekely</surname><given-names>L.</given-names></name><name><surname>Schulz</surname><given-names>T.F.</given-names></name></person-group><article-title>A Domain in the C-terminal region of latency-associated nuclear antigen 1 of Kaposi’s sarcoma-associated Herpesvirus affects transcriptional activation and binding to nuclear heterochromatin</article-title><source>J. Virol.</source><year>2003</year><volume>77</volume><fpage>7093</fpage><lpage>7100</lpage><pub-id pub-id-type="pmid">12768028</pub-id></element-citation></ref><ref id="B139-viruses-05-01374"><label>139.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Schowalter</surname><given-names>R.M.</given-names></name><name><surname>Jiao</surname><given-names>J.</given-names></name><name><surname>Buck</surname><given-names>C.B.</given-names></name><name><surname>You</surname><given-names>J.</given-names></name></person-group><article-title>Bromodomain protein Brd4 plays a key role in Merkel cell polyomavirus DNA replication</article-title><source>PLoS Pathog.</source><year>2012</year><volume>8</volume><fpage>e1003021</fpage><pub-id pub-id-type="doi">10.1371/journal.ppat.1003021</pub-id><pub-id pub-id-type="pmid">23144621</pub-id></element-citation></ref><ref id="B140-viruses-05-01374"><label>140.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>Z.</given-names></name><name><surname>Guo</surname><given-names>J.</given-names></name><name><surname>Wu</surname><given-names>Y.</given-names></name><name><surname>Zhou</surname><given-names>Q.</given-names></name></person-group><article-title>The BET bromodomain inhibitor JQ1 activates HIV latency through antagonizing Brd4 inhibition of Tat-transactivation</article-title><source>Nucleic Acids Res.</source><year>2013</year><volume>41</volume><fpage>277</fpage><lpage>287</lpage><pub-id pub-id-type="pmid">23087374</pub-id></element-citation></ref><ref id="B141-viruses-05-01374"><label>141.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Boehm</surname><given-names>D.</given-names></name><name><surname>Calvanese</surname><given-names>V.</given-names></name><name><surname>Dar</surname><given-names>R.D.</given-names></name><name><surname>Xing</surname><given-names>S.</given-names></name><name><surname>Schroeder</surname><given-names>S.</given-names></name><name><surname>Martins</surname><given-names>L.</given-names></name><name><surname>Aull</surname><given-names>K.</given-names></name><name><surname>Li</surname><given-names>P.C.</given-names></name><name><surname>Planelles</surname><given-names>V.</given-names></name><name><surname>Bradner</surname><given-names>J.E.</given-names></name><etal></etal></person-group><article-title>BET bromodomain-targeting compounds reactivate HIV from latency via a Tat-independent mechanism</article-title><source>Cell Cycle</source><year>2013</year><volume>12</volume><fpage>452</fpage><lpage>462</lpage><pub-id pub-id-type="doi">10.4161/cc.23309</pub-id><pub-id pub-id-type="pmid">23255218</pub-id></element-citation></ref><ref id="B142-viruses-05-01374"><label>142.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhu</surname><given-names>J.</given-names></name><name><surname>Gaiha</surname><given-names>G.D.</given-names></name><name><surname>John</surname><given-names>S.P.</given-names></name><name><surname>Pertel</surname><given-names>T.</given-names></name><name><surname>Chin</surname><given-names>C.R.</given-names></name><name><surname>Gao</surname><given-names>G.</given-names></name><name><surname>Qu</surname><given-names>H.</given-names></name><name><surname>Walker</surname><given-names>B.D.</given-names></name><name><surname>Elledge</surname><given-names>S.J.</given-names></name><name><surname>Brass</surname><given-names>A.L.</given-names></name></person-group><article-title>Reactivation of latent HIV-1 by inhibition of BRD4</article-title><source>Cell Rep.</source><year>2012</year><volume>2</volume><fpage>807</fpage><lpage>816</lpage><pub-id pub-id-type="doi">10.1016/j.celrep.2012.09.008</pub-id><pub-id pub-id-type="pmid">23041316</pub-id></element-citation></ref><ref id="B143-viruses-05-01374"><label>143.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Banerjee</surname><given-names>C.</given-names></name><name><surname>Archin</surname><given-names>N.</given-names></name><name><surname>Michaels</surname><given-names>D.</given-names></name><name><surname>Belkina</surname><given-names>A.C.</given-names></name><name><surname>Denis</surname><given-names>G.V.</given-names></name><name><surname>Bradner</surname><given-names>J.</given-names></name><name><surname>Sebastiani</surname><given-names>P.</given-names></name><name><surname>Margolis</surname><given-names>D.M.</given-names></name><name><surname>Montano</surname><given-names>M.</given-names></name></person-group><article-title>BET bromodomain inhibition as a novel strategy for reactivation of HIV-1</article-title><source>J. Leukoc. Biol.</source><year>2012</year><volume>92</volume><fpage>1147</fpage><lpage>1154</lpage><pub-id pub-id-type="doi">10.1189/jlb.0312165</pub-id><pub-id pub-id-type="pmid">22802445</pub-id></element-citation></ref></ref-list></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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