Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions
Identifieur interne : 002360 ( Istex/Corpus ); précédent : 002359; suivant : 002361Double‐strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions
Auteurs : Shengfang Jin ; David T. WeaverSource :
- The EMBO Journal [ 0261-4189 ] ; 1997-11-15.
English descriptors
- Teeft :
- Amino, Amino acid residues, Assay, Autoantigen, Bamhi, Binding, Binding activity, Binding properties, Biochemical features, Biol, Boubnov, Cdna, Cell extracts, Cell line, Cell lines, Cell lysates, Cells reconstituted, Chimera, Chimeric, Complementation, Core region, Derivative, Edta, Epitope, Expression vector, Hdf1, Heterodimerization, Higher mobility, Immunoprecipitation, Kinase, Kinase buffer, Lieber, Lysates, Lysis, Lysis buffer, Monoclonal, Monoclonal antibody, Mutagenesis, Mutant, Mutation, Mutational analysis, Nacl, Natl acad, Noti, Nucleic acids, Pefpuro, Peptide, Phosphoamino acid analysis, Phosphorylated, Phosphorylation, Primer, Protein kinase, Recombination, Reconstituted, Repair, Repair defects, Saccharomyces cerevisiae, Serine, Stably, Stably transfected, Subunit, Truncation, Truncation mutants, Yeast, Yeast expression vector.
Abstract
Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. These studies reveal Ku70 features required for double‐strand break repair.
Url:
DOI: 10.1093/emboj/16.22.6874
Links to Exploration step
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<front><div type="abstract">Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. These studies reveal Ku70 features required for double‐strand break repair.</div>
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<profileDesc><abstract style="main"><p>Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair <hi rend="italic">in vivo</hi>
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<abstract>Heterodimers of the 70 and 80 kDa Ku autoantigens (Ku70 and Ku80) activate the DNA‐dependent protein kinase (DNA‐PK). Mutations in any of the three subunits of this protein kinase (Ku70, Ku80 and DNA‐PKcs) lead to sensitivity to ionizing radiation (IR) and to DNA double‐strand breaks, and V(D)J recombination product formation defects. Here we show that the IR repair, DNA end binding and DNA‐PK defects in Ku70−/− embryonic stem cells can be counteracted by introducing epitope‐tagged wild‐type Ku70 cDNA. Truncations and chimeras of Ku70 were used to identify the regions necessary for DNA end binding and IR repair. Site‐specific mutational analysis revealed a core region of Ku70 responsible for DNA end binding and heterodimerization. The propensity for Ku70 to associate with Ku80 and to bind DNA correlates with the ability to activate DNA‐PK, although two mutants showed that the roles of Ku70 in DNA‐PK activation and IR repair are separate. Mutation of DNA‐PK autophosphorylation sites and other structural motifs in Ku70 showed that these sites are not necessary for IR repair in vivo. These studies reveal Ku70 features required for double‐strand break repair.</abstract>
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<number>22</number>
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<end>6885</end>
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<relatedItem type="references" displayLabel="embj7590657-citation-0001"><titleInfo><title>The nuclear serine/threonine protein kinase DNA‐PK</title>
</titleInfo>
<name type="personal"><namePart type="given">CW</namePart>
<namePart type="family">Anderson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Anderson CW and Lees‐Miller SP (1992) The nuclear serine/threonine protein kinase DNA‐PK. Crit Rev Euk Gene Expr, 2, 283–314.</note>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>2</number>
</detail>
<extent unit="pages"><start>283</start>
<end>314</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Crit Rev Euk Gene Expr</title>
</titleInfo>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>2</number>
</detail>
<extent unit="pages"><start>283</start>
<end>314</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0002"><titleInfo><title>Defective DNA‐dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation</title>
</titleInfo>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Blunt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Blunt T et al. (1995) Defective DNA‐dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation. Cell, 80, 813–823.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>80</number>
</detail>
<extent unit="pages"><start>813</start>
<end>823</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Cell</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>80</number>
</detail>
<extent unit="pages"><start>813</start>
<end>823</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0003"><titleInfo><title>Identification of a Saccharomyces cerevisiae Ku80 homologue: roles in DNA double strand break rejoining and in telomeric maintenance</title>
</titleInfo>
<name type="personal"><namePart type="given">SJ</namePart>
<namePart type="family">Bolton</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Jackson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Bolton SJ and Jackson SP (1996) Identification of a Saccharomyces cerevisiae Ku80 homologue: roles in DNA double strand break rejoining and in telomeric maintenance. Nucleic Acids Res, 24, 4639–4648.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages"><start>4639</start>
<end>4648</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages"><start>4639</start>
<end>4648</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0004"><titleInfo><title>Scid cells are deficient in Ku and RPA phosphorylation by the DNA‐dependent protein kinase</title>
</titleInfo>
<name type="personal"><namePart type="given">NV</namePart>
<namePart type="family">Boubnov</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DT</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Boubnov NV and Weaver DT (1995a) Scid cells are deficient in Ku and RPA phosphorylation by the DNA‐dependent protein kinase. Mol Cell Biol, 15, 5700–5706.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>15</number>
</detail>
<extent unit="pages"><start>5700</start>
<end>5706</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>15</number>
</detail>
<extent unit="pages"><start>5700</start>
<end>5706</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0005"><titleInfo><title>Complementation of the ionizing radiation sensitivity, DNA end binding, and V(D)J recombination defects of double‐strand break repair mutants by the p86 Ku autoantigen</title>
</titleInfo>
<name type="personal"><namePart type="given">NV</namePart>
<namePart type="family">Boubnov</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Boubnov NV et al. (1995b) Complementation of the ionizing radiation sensitivity, DNA end binding, and V(D)J recombination defects of double‐strand break repair mutants by the p86 Ku autoantigen. Proc Natl Acad Sci USA, 92, 890–894.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>92</number>
</detail>
<extent unit="pages"><start>890</start>
<end>894</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>92</number>
</detail>
<extent unit="pages"><start>890</start>
<end>894</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0006"><titleInfo><title>DNA‐dependent ATPase from HeLa cells is related to human Ku autoantigen</title>
</titleInfo>
<name type="personal"><namePart type="given">QP</namePart>
<namePart type="family">Cao</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Pitt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J</namePart>
<namePart type="family">Leszyk</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">EF</namePart>
<namePart type="family">Baril</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Cao QP, Pitt S, Leszyk J and Baril EF (1994) DNA‐dependent ATPase from HeLa cells is related to human Ku autoantigen. Biochemistry, 33, 8548–8557.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>33</number>
</detail>
<extent unit="pages"><start>8548</start>
<end>8557</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Biochemistry</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>33</number>
</detail>
<extent unit="pages"><start>8548</start>
<end>8557</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0007"><titleInfo><title>The DNA‐dependent protein kinase is inactivated by autophosphorylation of the catalytic subunit</title>
</titleInfo>
<name type="personal"><namePart type="given">DW</namePart>
<namePart type="family">Chan</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Chan DW and Lees‐Miller SP (1996) The DNA‐dependent protein kinase is inactivated by autophosphorylation of the catalytic subunit. J Biol Chem, 271, 8936–8941.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>271</number>
</detail>
<extent unit="pages"><start>8936</start>
<end>8941</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>271</number>
</detail>
<extent unit="pages"><start>8936</start>
<end>8941</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0008"><titleInfo><title>Role of a major autoepitope in forming the DNA binding site of the p70(Ku) antigen</title>
</titleInfo>
<name type="personal"><namePart type="given">C</namePart>
<namePart type="family">Chou</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J</namePart>
<namePart type="family">Wang</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Knoth</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">W</namePart>
<namePart type="family">Reeves</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Chou C, Wang J, Knoth M and Reeves W (1992) Role of a major autoepitope in forming the DNA binding site of the p70(Ku) antigen. J Exp Med, 175, 1677–1684.</note>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>175</number>
</detail>
<extent unit="pages"><start>1677</start>
<end>1684</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Exp Med</title>
</titleInfo>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>175</number>
</detail>
<extent unit="pages"><start>1677</start>
<end>1684</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0009"><titleInfo><title>Coligan JE, Kruisbeek AM, Margulies DH, Shevach EM and Strober W. (1995) In Coico,R. (ed.), Current Protocols in Immunology. Volume I, John Wiley and Sons.</title>
</titleInfo>
<note type="citation/reference">Coligan JE, Kruisbeek AM, Margulies DH, Shevach EM and Strober W. (1995) In Coico,R. (ed.), Current Protocols in Immunology. Volume I, John Wiley and Sons.</note>
<name type="personal"><namePart type="given">JE</namePart>
<namePart type="family">Coligan</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">AM</namePart>
<namePart type="family">Kruisbeek</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DH</namePart>
<namePart type="family">Margulies</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">EM</namePart>
<namePart type="family">Shevach</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">W</namePart>
<namePart type="family">Strober</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>book</genre>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>I</number>
</detail>
</part>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0010"><titleInfo><title>Ku86 defines the genetic defect and restores X‐ray resistance and V(D)J recombination to complementation group 5 hamster cell mutants</title>
</titleInfo>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Errami</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">V</namePart>
<namePart type="family">Smider</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">WK</namePart>
<namePart type="family">Rathmell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DM</namePart>
<namePart type="family">He</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">EA</namePart>
<namePart type="family">Hendrickson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MZ</namePart>
<namePart type="family">Zdzienicka</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">G</namePart>
<namePart type="family">Chu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Errami A, Smider V, Rathmell WK, He DM, Hendrickson EA, Zdzienicka MZ and Chu G (1996) Ku86 defines the genetic defect and restores X‐ray resistance and V(D)J recombination to complementation group 5 hamster cell mutants. Mol Cell Biol, 16, 1519–1526.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>1519</start>
<end>1526</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>1519</start>
<end>1526</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0011"><titleInfo><title>A putative homologue of the human autoantigen Ku from Saccharomyces cerevisiae</title>
</titleInfo>
<name type="personal"><namePart type="given">H</namePart>
<namePart type="family">Feldmann</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">EL</namePart>
<namePart type="family">Winnacker</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Feldmann H and Winnacker EL (1993) A putative homologue of the human autoantigen Ku from Saccharomyces cerevisiae. J Biol Chem, 268, 12895–12900.</note>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>268</number>
</detail>
<extent unit="pages"><start>12895</start>
<end>12900</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>268</number>
</detail>
<extent unit="pages"><start>12895</start>
<end>12900</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0012"><titleInfo><title>DNA‐dependent protein kinase activity is absent in xrs‐6 cells: implications for site‐specific recombination and DNA double‐strand break repair</title>
</titleInfo>
<name type="personal"><namePart type="given">NJ</namePart>
<namePart type="family">Finnie</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">TM</namePart>
<namePart type="family">Gottlieb</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Blunt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">PA</namePart>
<namePart type="family">Jeggo</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Jackson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Finnie NJ, Gottlieb TM, Blunt T, Jeggo PA and Jackson SP (1995) DNA‐dependent protein kinase activity is absent in xrs‐6 cells: implications for site‐specific recombination and DNA double‐strand break repair. Proc Natl Acad Sci USA, 92, 320–324.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>92</number>
</detail>
<extent unit="pages"><start>320</start>
<end>324</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>92</number>
</detail>
<extent unit="pages"><start>320</start>
<end>324</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0013"><titleInfo><title>Absence of a Ku‐like DNA end binding activity in the xrs double‐strand DNA repair‐deficient mutant</title>
</titleInfo>
<name type="personal"><namePart type="given">RC</namePart>
<namePart type="family">Getts</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">TD</namePart>
<namePart type="family">Stamato</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Getts RC and Stamato TD (1994) Absence of a Ku‐like DNA end binding activity in the xrs double‐strand DNA repair‐deficient mutant. J Biol Chem, 269, 15981–15984.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>269</number>
</detail>
<extent unit="pages"><start>15981</start>
<end>15984</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>269</number>
</detail>
<extent unit="pages"><start>15981</start>
<end>15984</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0014"><titleInfo><title>Sequence‐specific DNA binding by Ku autoantigen and its effects on transcription</title>
</titleInfo>
<name type="personal"><namePart type="given">W</namePart>
<namePart type="family">Giffin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">H</namePart>
<namePart type="family">Torrance</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DJ</namePart>
<namePart type="family">Rodda</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">GG</namePart>
<namePart type="family">Prefontaine</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">L</namePart>
<namePart type="family">Pope</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">RJG</namePart>
<namePart type="family">Hache</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Giffin W, Torrance H, Rodda DJ, Prefontaine GG, Pope L and Hache RJG (1996) Sequence‐specific DNA binding by Ku autoantigen and its effects on transcription. Nature, 380, 265–268.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>380</number>
</detail>
<extent unit="pages"><start>265</start>
<end>268</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nature</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>380</number>
</detail>
<extent unit="pages"><start>265</start>
<end>268</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0015"><titleInfo><title>Ku polypeptides synthesized in vitro assemble into complexes which recognize ends of double‐stranded DNA</title>
</titleInfo>
<name type="personal"><namePart type="given">AJ</namePart>
<namePart type="family">Griffith</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">PR</namePart>
<namePart type="family">Blier</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Mimori</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">JA</namePart>
<namePart type="family">Hardin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Griffith AJ, Blier PR, Mimori T and Hardin JA (1992) Ku polypeptides synthesized in vitro assemble into complexes which recognize ends of double‐stranded DNA. J Biol Chem, 267, 331–338.</note>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>267</number>
</detail>
<extent unit="pages"><start>331</start>
<end>338</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>267</number>
</detail>
<extent unit="pages"><start>331</start>
<end>338</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0016"><titleInfo><title>Ku70‐deficient ES cells have increase ionizing radiosensitivity, defective DNA end binding activity, and inability to support V(D)J recombination</title>
</titleInfo>
<name type="personal"><namePart type="given">Y</namePart>
<namePart type="family">Gu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Jin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Y</namePart>
<namePart type="family">Gao</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DT</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">FW</namePart>
<namePart type="family">Alt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Gu Y, Jin S, Gao Y, Weaver DT and Alt FW (1997) Ku70‐deficient ES cells have increase ionizing radiosensitivity, defective DNA end binding activity, and inability to support V(D)J recombination. Proc Natl Acad Sci USA, 94, 8076–8081.</note>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>94</number>
</detail>
<extent unit="pages"><start>8076</start>
<end>8081</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title>
</titleInfo>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>94</number>
</detail>
<extent unit="pages"><start>8076</start>
<end>8081</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0017"><titleInfo><title>DNA‐dependent protein kinase catalytic subunit: a relative of phosphatidylinositol 3‐kinase and the ataxia telangiectasia gene product</title>
</titleInfo>
<name type="personal"><namePart type="given">KO</namePart>
<namePart type="family">Hartley</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D</namePart>
<namePart type="family">Gell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">GCM</namePart>
<namePart type="family">Smith</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">H</namePart>
<namePart type="family">Zhang</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">N</namePart>
<namePart type="family">Dvecha</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MA</namePart>
<namePart type="family">Connelly</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Admon</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">CW</namePart>
<namePart type="family">Anderson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Jackson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Hartley KO, Gell D, Smith GCM, Zhang H, Dvecha N, Connelly MA, Admon A, Lees‐Miller SP, Anderson CW and Jackson SP (1995) DNA‐dependent protein kinase catalytic subunit: a relative of phosphatidylinositol 3‐kinase and the ataxia telangiectasia gene product. Cell, 82, 849–856.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>82</number>
</detail>
<extent unit="pages"><start>849</start>
<end>856</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Cell</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>82</number>
</detail>
<extent unit="pages"><start>849</start>
<end>856</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0018"><titleInfo><title>Functions of the DNA‐dependent protein kinase</title>
</titleInfo>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Jin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Inoue</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DT</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Jin S, Inoue S and Weaver DT (1997a) Functions of the DNA‐dependent protein kinase. Cancer Surveys, 29, 221–261.</note>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages"><start>221</start>
<end>261</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Cancer Surveys</title>
</titleInfo>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages"><start>221</start>
<end>261</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0019"><titleInfo><title>DNA‐dependent protein kinase catalytic subunit: binding of the Ku activator and c‐Abl tyrosine kinase proteins</title>
</titleInfo>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Jin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Kharbanda</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D</namePart>
<namePart type="family">Kufe</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">B</namePart>
<namePart type="family">Mayer</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DT</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Jin S, Kharbanda S, Kufe D, Mayer B and Weaver DT (1997b) DNA‐dependent protein kinase catalytic subunit: binding of the Ku activator and c‐Abl tyrosine kinase proteins. J Biol Chem, 272, 24763–24766.</note>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>272</number>
</detail>
<extent unit="pages"><start>24763</start>
<end>24766</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>272</number>
</detail>
<extent unit="pages"><start>24763</start>
<end>24766</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0020"><titleInfo><title>Functional interactions of the DNA‐dependent protein kinase and the c‐Abl protein tyrosine kinase in the response to DNA damage</title>
</titleInfo>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Kharbanda</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">P</namePart>
<namePart type="family">Pandey</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Jin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Inoue</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Bharti</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Z‐M</namePart>
<namePart type="family">Yuan</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">R</namePart>
<namePart type="family">Weichselbaum</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D</namePart>
<namePart type="family">Kufe</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kharbanda S, Pandey P, Jin S, Inoue S, Bharti A, Yuan Z‐M, Weichselbaum R, Weaver D and Kufe D (1997) Functional interactions of the DNA‐dependent protein kinase and the c‐Abl protein tyrosine kinase in the response to DNA damage. Nature, 386, 732–735.</note>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>386</number>
</detail>
<extent unit="pages"><start>732</start>
<end>735</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nature</title>
</titleInfo>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>386</number>
</detail>
<extent unit="pages"><start>732</start>
<end>735</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0021"><titleInfo><title>A common set of conserved motifs in a vast variety of putative nucleic acid‐dependent ATPases including MCM proteins involved in the initiation of eukaryotic DNA replication</title>
</titleInfo>
<name type="personal"><namePart type="given">E</namePart>
<namePart type="family">Koonin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Koonin E (1993) A common set of conserved motifs in a vast variety of putative nucleic acid‐dependent ATPases including MCM proteins involved in the initiation of eukaryotic DNA replication. Nucleic Acids Res, 21, 2541–2547.</note>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>21</number>
</detail>
<extent unit="pages"><start>2541</start>
<end>2547</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title>
</titleInfo>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>21</number>
</detail>
<extent unit="pages"><start>2541</start>
<end>2547</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0022"><titleInfo><title>Human cells contain a DNA‐activated protein kinase that phosphorylates simian virus 40 T antigen, mouse p53, and the human Ku autoantigen</title>
</titleInfo>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Y</namePart>
<namePart type="family">Chen</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">CW</namePart>
<namePart type="family">Anderson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lees‐Miller SP, Chen Y and Anderson CW (1990) Human cells contain a DNA‐activated protein kinase that phosphorylates simian virus 40 T antigen, mouse p53, and the human Ku autoantigen. Mol Cell Biol, 10, 6472–6481.</note>
<part><date>1990</date>
<detail type="volume"><caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages"><start>6472</start>
<end>6481</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1990</date>
<detail type="volume"><caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages"><start>6472</start>
<end>6481</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0023"><titleInfo><title>Human DNA‐activated protein kinase phosphorylates serines 15 and 37 in the amino‐terminal transactivation domain of human p53</title>
</titleInfo>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">K</namePart>
<namePart type="family">Sakaguchi</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SJ</namePart>
<namePart type="family">Ullrich</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">E</namePart>
<namePart type="family">Appella</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">CW</namePart>
<namePart type="family">Anderson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lees‐Miller SP, Sakaguchi K, Ullrich SJ, Appella E and Anderson CW (1992) Human DNA‐activated protein kinase phosphorylates serines 15 and 37 in the amino‐terminal transactivation domain of human p53. Mol Cell Biol, 12, 5041–5049.</note>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>12</number>
</detail>
<extent unit="pages"><start>5041</start>
<end>5049</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>12</number>
</detail>
<extent unit="pages"><start>5041</start>
<end>5049</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0024"><titleInfo><title>Absence of p350 subunit of DNA‐activated protein kinase from a radiosensitive human cell line</title>
</titleInfo>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Lees‐Miller</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">R</namePart>
<namePart type="family">Godbout</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DW</namePart>
<namePart type="family">Chan</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Weinfeld</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">RS</namePart>
<namePart type="family">Day</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">GM</namePart>
<namePart type="family">Barron</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J</namePart>
<namePart type="family">Allalunis‐Turner</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lees‐Miller SP, Godbout R, Chan DW, Weinfeld M, Day RS, Barron GM and Allalunis‐Turner J (1995) Absence of p350 subunit of DNA‐activated protein kinase from a radiosensitive human cell line. Science, 267, 1183–1185.</note>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>267</number>
</detail>
<extent unit="pages"><start>1183</start>
<end>1185</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Science</title>
</titleInfo>
<part><date>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>267</number>
</detail>
<extent unit="pages"><start>1183</start>
<end>1185</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0025"><titleInfo><title>Chromosomal double‐strand break repair in Ku80 deficient cells</title>
</titleInfo>
<name type="personal"><namePart type="given">F</namePart>
<namePart type="family">Liang</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">P</namePart>
<namePart type="family">Romanienko</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">P</namePart>
<namePart type="family">Jeggo</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Jasin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Liang F, Romanienko P, Weaver D, Jeggo P and Jasin M (1996) Chromosomal double‐strand break repair in Ku80 deficient cells. Proc Natl Acad Sci USA, 93, 8929–8933.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>93</number>
</detail>
<extent unit="pages"><start>8929</start>
<end>8933</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>93</number>
</detail>
<extent unit="pages"><start>8929</start>
<end>8933</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0026"><titleInfo><title>Tying loose ends: roles of Ku and DNA‐dependent protein kinase in the repair of double‐strand breaks</title>
</titleInfo>
<name type="personal"><namePart type="given">MR</namePart>
<namePart type="family">Lieber</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">U</namePart>
<namePart type="family">Grawunder</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">X</namePart>
<namePart type="family">Wu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Yaneva</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lieber MR, Grawunder U, Wu X and Yaneva M (1997) Tying loose ends: roles of Ku and DNA‐dependent protein kinase in the repair of double‐strand breaks. Curr Opin Genet Dev, 7, 99–104.</note>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages"><start>99</start>
<end>104</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Curr Opin Genet Dev</title>
</titleInfo>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages"><start>99</start>
<end>104</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0027"><titleInfo><title>The DNA‐dependent protein kinase: a matter of life and (cell) death</title>
</titleInfo>
<name type="personal"><namePart type="given">K</namePart>
<namePart type="family">McConnell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">WS</namePart>
<namePart type="family">Dynan</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">McConnell K and Dynan WS (1996) The DNA‐dependent protein kinase: a matter of life and (cell) death. Curr Opin Cell Biol, 12, 325–330.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>12</number>
</detail>
<extent unit="pages"><start>325</start>
<end>330</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Curr Opin Cell Biol</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>12</number>
</detail>
<extent unit="pages"><start>325</start>
<end>330</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0028"><titleInfo><title>Mutations in two Ku homologs define a DNA end‐joining repair pathway in Saccharomyces cerevisiae</title>
</titleInfo>
<name type="personal"><namePart type="given">GT</namePart>
<namePart type="family">Milne</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Jin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">K</namePart>
<namePart type="family">Shannon</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DT</namePart>
<namePart type="family">Weaver</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Milne GT, Jin S, Shannon K and Weaver DT (1996) Mutations in two Ku homologs define a DNA end‐joining repair pathway in Saccharomyces cerevisiae. Mol Cell Biol, 16, 4189–4198.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>4189</start>
<end>4198</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>4189</start>
<end>4198</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0029"><titleInfo><title>Characterization of a high molecular weight acidic nuclear protein recognized by autoantibodies from patients with polymyositis–schleroderma overlap</title>
</titleInfo>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Mimori</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Akizuki</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">H</namePart>
<namePart type="family">Yamagata</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Inada</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Yoshida</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Homma</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Mimori T, Akizuki M, Yamagata H, Inada S, Yoshida S and Homma M (1981) Characterization of a high molecular weight acidic nuclear protein recognized by autoantibodies from patients with polymyositis–schleroderma overlap. J Clin Invest, 68, 611–620.</note>
<part><date>1981</date>
<detail type="volume"><caption>vol.</caption>
<number>68</number>
</detail>
<extent unit="pages"><start>611</start>
<end>620</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Clin Invest</title>
</titleInfo>
<part><date>1981</date>
<detail type="volume"><caption>vol.</caption>
<number>68</number>
</detail>
<extent unit="pages"><start>611</start>
<end>620</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0030"><titleInfo><title>pEF‐BOS, a powerful mammalian expression vector</title>
</titleInfo>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Mizushima</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S</namePart>
<namePart type="family">Nagata</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Mizushima S and Nagata S (1990) pEF‐BOS, a powerful mammalian expression vector. Nucleic Acids Res, 18, 5332.</note>
<part><date>1990</date>
<detail type="volume"><caption>vol.</caption>
<number>18</number>
</detail>
<extent unit="pages"><start>5332</start>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title>
</titleInfo>
<part><date>1990</date>
<detail type="volume"><caption>vol.</caption>
<number>18</number>
</detail>
<extent unit="pages"><start>5332</start>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0031"><titleInfo><title>Requirement for Ku80 in growth and immunoglobulin V(D)J recombination</title>
</titleInfo>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Nussenzweig</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">C</namePart>
<namePart type="family">Chen</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">V</namePart>
<namePart type="family">da Costa Soares</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Sanchez</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">K</namePart>
<namePart type="family">Sokol</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MC</namePart>
<namePart type="family">Nussenzweig</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">GC</namePart>
<namePart type="family">Li</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Nussenzweig A, Chen C da Costa Soares V Sanchez M, Sokol K, Nussenzweig MC and Li GC (1996) Requirement for Ku80 in growth and immunoglobulin V(D)J recombination. Nature, 382, 551–555.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>382</number>
</detail>
<extent unit="pages"><start>551</start>
<end>555</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nature</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>382</number>
</detail>
<extent unit="pages"><start>551</start>
<end>555</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0032"><titleInfo><title>The DNA‐binding protein Hdf1p (a putative Ku homolog) is required for maintaining normal teleomere length in Saccharomyces cerevisiae</title>
</titleInfo>
<name type="personal"><namePart type="given">SE</namePart>
<namePart type="family">Porter</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">PW</namePart>
<namePart type="family">Greenwell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">KB</namePart>
<namePart type="family">Ritchie</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">TD</namePart>
<namePart type="family">Petes</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Porter SE, Greenwell PW, Ritchie KB and Petes TD (1996) The DNA‐binding protein Hdf1p (a putative Ku homolog) is required for maintaining normal teleomere length in Saccharomyces cerevisiae. Nucleic Acids Res, 24, 582–585.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages"><start>582</start>
<end>585</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages"><start>582</start>
<end>585</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0033"><titleInfo><title>A DNA end‐binding factor involved in double‐strand break repair and V(D)J recombination</title>
</titleInfo>
<name type="personal"><namePart type="given">WK</namePart>
<namePart type="family">Rathmell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">G</namePart>
<namePart type="family">Chu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Rathmell WK and Chu G (1994) A DNA end‐binding factor involved in double‐strand break repair and V(D)J recombination. Mol Cell Biol, 14, 4741–4748.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages"><start>4741</start>
<end>4748</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages"><start>4741</start>
<end>4748</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0034"><titleInfo><title>Molecular cloning of cDNA encoding the p70 (Ku) lupus autoantigen</title>
</titleInfo>
<name type="personal"><namePart type="given">WH</namePart>
<namePart type="family">Reeves</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">ZM</namePart>
<namePart type="family">Sthoeger</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Reeves WH and Sthoeger ZM (1989) Molecular cloning of cDNA encoding the p70 (Ku) lupus autoantigen. J Biol Chem, 264, 5047–5052.</note>
<part><date>1989</date>
<detail type="volume"><caption>vol.</caption>
<number>264</number>
</detail>
<extent unit="pages"><start>5047</start>
<end>5052</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>J Biol Chem</title>
</titleInfo>
<part><date>1989</date>
<detail type="volume"><caption>vol.</caption>
<number>264</number>
</detail>
<extent unit="pages"><start>5047</start>
<end>5052</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0035"><titleInfo><title>Restoration of X‐ray resistance and V(D)J recombination in mutant cells by Ku cDNA</title>
</titleInfo>
<name type="personal"><namePart type="given">V</namePart>
<namePart type="family">Smider</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">WK</namePart>
<namePart type="family">Rathmell</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MR</namePart>
<namePart type="family">Lieber</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">G</namePart>
<namePart type="family">Chu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Smider V, Rathmell WK, Lieber MR and Chu G (1994) Restoration of X‐ray resistance and V(D)J recombination in mutant cells by Ku cDNA. Science, 266, 288–291.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>266</number>
</detail>
<extent unit="pages"><start>288</start>
<end>291</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Science</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>266</number>
</detail>
<extent unit="pages"><start>288</start>
<end>291</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0036"><titleInfo><title>DNA‐dependent protein kinase (Ku protein‐p350 complex) assembles on double‐stranded DNA</title>
</titleInfo>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Suwa</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Hirakata</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Y</namePart>
<namePart type="family">Takeda</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SA</namePart>
<namePart type="family">Jesch</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Mimori</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">JA</namePart>
<namePart type="family">Hardin</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Suwa A, Hirakata M, Takeda Y, Jesch SA, Mimori T and Hardin JA (1994) DNA‐dependent protein kinase (Ku protein‐p350 complex) assembles on double‐stranded DNA. Proc Natl Acad Sci USA, 91, 6904–6908.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>91</number>
</detail>
<extent unit="pages"><start>6904</start>
<end>6908</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>91</number>
</detail>
<extent unit="pages"><start>6904</start>
<end>6908</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0037"><titleInfo><title>Ku80: product of the XRCC5 gene and its role in DNA repair and V(D)J recombination</title>
</titleInfo>
<name type="personal"><namePart type="given">G</namePart>
<namePart type="family">Taccioli</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">TM</namePart>
<namePart type="family">Gottlieb</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">T</namePart>
<namePart type="family">Blunt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">A</namePart>
<namePart type="family">Priestly</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J</namePart>
<namePart type="family">Demengeot</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">R</namePart>
<namePart type="family">Mizuta</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">AR</namePart>
<namePart type="family">Lehmann</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">FW</namePart>
<namePart type="family">Alt</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SP</namePart>
<namePart type="family">Jackson</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">PA</namePart>
<namePart type="family">Jeggo</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Taccioli G, Gottlieb TM, Blunt T, Priestly A, Demengeot J, Mizuta R, Lehmann AR, Alt FW, Jackson SP and Jeggo PA (1994) Ku80: product of the XRCC5 gene and its role in DNA repair and V(D)J recombination. Science, 265, 1442–1445.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>265</number>
</detail>
<extent unit="pages"><start>1442</start>
<end>1445</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Science</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>265</number>
</detail>
<extent unit="pages"><start>1442</start>
<end>1445</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0038"><titleInfo><title>Human DNA helicase II: a novel DNA unwinding enzyme identified as the Ku autoantigen</title>
</titleInfo>
<name type="personal"><namePart type="given">N</namePart>
<namePart type="family">Tuteja</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Tuteja N et al. (1994) Human DNA helicase II: a novel DNA unwinding enzyme identified as the Ku autoantigen. EMBO J, 13, 4991–5001.</note>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages"><start>4991</start>
<end>5001</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>EMBO J</title>
</titleInfo>
<part><date>1994</date>
<detail type="volume"><caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages"><start>4991</start>
<end>5001</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0039"><titleInfo><title>Protein–protein and protein–DNA interaction regions within the DNA end‐binding protein Ku70–Ku86</title>
</titleInfo>
<name type="personal"><namePart type="given">X</namePart>
<namePart type="family">Wu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Lieber</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Wu X and Lieber M (1996) Protein–protein and protein–DNA interaction regions within the DNA end‐binding protein Ku70–Ku86. Mol Cell Biol, 16, 5186–5193.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>5186</start>
<end>5193</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Mol Cell Biol</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages"><start>5186</start>
<end>5193</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0040"><titleInfo><title>On the mechanisms of Ku protein binding to DNA</title>
</titleInfo>
<name type="personal"><namePart type="given">W‐W</namePart>
<namePart type="family">Zhang</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Yaneva</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Zhang W‐W and Yaneva M (1992) On the mechanisms of Ku protein binding to DNA. Biochem Biophys Res Commun, 186, 574–579.</note>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>186</number>
</detail>
<extent unit="pages"><start>574</start>
<end>579</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Biochem Biophys Res Commun</title>
</titleInfo>
<part><date>1992</date>
<detail type="volume"><caption>vol.</caption>
<number>186</number>
</detail>
<extent unit="pages"><start>574</start>
<end>579</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0041"><titleInfo><title>Reduced sulphydryl groups are required for DNA binding of Ku protein</title>
</titleInfo>
<name type="personal"><namePart type="given">WW</namePart>
<namePart type="family">Zhang</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M</namePart>
<namePart type="family">Yaneva</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Zhang WW and Yaneva M (1993) Reduced sulphydryl groups are required for DNA binding of Ku protein. Biochem J, 293, 769–774.</note>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>293</number>
</detail>
<extent unit="pages"><start>769</start>
<end>774</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Biochem J</title>
</titleInfo>
<part><date>1993</date>
<detail type="volume"><caption>vol.</caption>
<number>293</number>
</detail>
<extent unit="pages"><start>769</start>
<end>774</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="embj7590657-citation-0042"><titleInfo><title>Ku86‐deficient mice exhibit severe combined immunodeficiency and defective processing of V(D)J recombination intermediates</title>
</titleInfo>
<name type="personal"><namePart type="given">C</namePart>
<namePart type="family">Zhu</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MA</namePart>
<namePart type="family">Bogue</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">D‐S</namePart>
<namePart type="family">Lim</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">P</namePart>
<namePart type="family">Hasty</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">DB</namePart>
<namePart type="family">Roth</namePart>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Zhu C, Bogue MA, Lim D‐S, Hasty P and Roth DB (1996) Ku86‐deficient mice exhibit severe combined immunodeficiency and defective processing of V(D)J recombination intermediates. Cell, 86, 379–389.</note>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>86</number>
</detail>
<extent unit="pages"><start>379</start>
<end>389</end>
</extent>
</part>
<relatedItem type="host"><titleInfo><title>Cell</title>
</titleInfo>
<part><date>1996</date>
<detail type="volume"><caption>vol.</caption>
<number>86</number>
</detail>
<extent unit="pages"><start>379</start>
<end>389</end>
</extent>
</part>
</relatedItem>
</relatedItem>
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