Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</title><author><name sortKey="Zencak, Dusan" sort="Zencak, Dusan" uniqKey="Zencak D" first="Dusan" last="Zencak">Dusan Zencak</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Schouwey, Karine" sort="Schouwey, Karine" uniqKey="Schouwey K" first="Karine" last="Schouwey">Karine Schouwey</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Chen, Danian" sort="Chen, Danian" uniqKey="Chen D" first="Danian" last="Chen">Danian Chen</name><affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>, Toronto, ON,<country>Canada</country> M5T 2S8;</nlm:aff></affiliation></author><author><name sortKey="Ekstrom, Per" sort="Ekstrom, Per" uniqKey="Ekstrom P" first="Per" last="Ekström">Per Ekström</name><affiliation><nlm:aff wicri:cut="; and" id="aff3">Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>, SE-221 84 Lund,<country>Sweden</country></nlm:aff></affiliation></author><author><name sortKey="Tanger, Ellen" sort="Tanger, Ellen" uniqKey="Tanger E" first="Ellen" last="Tanger">Ellen Tanger</name><affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>, 1066 CX, Amsterdam,<country>The Netherlands</country></nlm:aff></affiliation></author><author><name sortKey="Bremner, Rod" sort="Bremner, Rod" uniqKey="Bremner R" first="Rod" last="Bremner">Rod Bremner</name><affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>, Toronto, ON,<country>Canada</country> M5T 2S8;</nlm:aff></affiliation></author><author><name sortKey="Van Lohuizen, Maarten" sort="Van Lohuizen, Maarten" uniqKey="Van Lohuizen M" first="Maarten" last="Van Lohuizen">Maarten Van Lohuizen</name><affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>, 1066 CX, Amsterdam,<country>The Netherlands</country></nlm:aff></affiliation></author><author><name sortKey="Arsenijevic, Yvan" sort="Arsenijevic, Yvan" uniqKey="Arsenijevic Y" first="Yvan" last="Arsenijevic">Yvan Arsenijevic</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23359713</idno><idno type="pmc">3574927</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3574927</idno><idno type="RBID">PMC:3574927</idno><idno type="doi">10.1073/pnas.1108297110</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000664</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000664</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</title><author><name sortKey="Zencak, Dusan" sort="Zencak, Dusan" uniqKey="Zencak D" first="Dusan" last="Zencak">Dusan Zencak</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Schouwey, Karine" sort="Schouwey, Karine" uniqKey="Schouwey K" first="Karine" last="Schouwey">Karine Schouwey</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Chen, Danian" sort="Chen, Danian" uniqKey="Chen D" first="Danian" last="Chen">Danian Chen</name><affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>, Toronto, ON,<country>Canada</country> M5T 2S8;</nlm:aff></affiliation></author><author><name sortKey="Ekstrom, Per" sort="Ekstrom, Per" uniqKey="Ekstrom P" first="Per" last="Ekström">Per Ekström</name><affiliation><nlm:aff wicri:cut="; and" id="aff3">Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>, SE-221 84 Lund,<country>Sweden</country></nlm:aff></affiliation></author><author><name sortKey="Tanger, Ellen" sort="Tanger, Ellen" uniqKey="Tanger E" first="Ellen" last="Tanger">Ellen Tanger</name><affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>, 1066 CX, Amsterdam,<country>The Netherlands</country></nlm:aff></affiliation></author><author><name sortKey="Bremner, Rod" sort="Bremner, Rod" uniqKey="Bremner R" first="Rod" last="Bremner">Rod Bremner</name><affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>, Toronto, ON,<country>Canada</country> M5T 2S8;</nlm:aff></affiliation></author><author><name sortKey="Van Lohuizen, Maarten" sort="Van Lohuizen, Maarten" uniqKey="Van Lohuizen M" first="Maarten" last="Van Lohuizen">Maarten Van Lohuizen</name><affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>, 1066 CX, Amsterdam,<country>The Netherlands</country></nlm:aff></affiliation></author><author><name sortKey="Arsenijevic, Yvan" sort="Arsenijevic, Yvan" uniqKey="Arsenijevic Y" first="Yvan" last="Arsenijevic">Yvan Arsenijevic</name><affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</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 epigenetic regulator Bmi1 controls proliferation in many organs. Reexpression of cell cycle proteins such as cyclin-dependent kinases (CDKs) is a hallmark of neuronal apoptosis in neurodegenerative diseases. Here we address the potential role of Bmi1 as a key regulator of cell cycle proteins during neuronal apoptosis. We show that several cell cycle proteins are expressed in different models of retinal degeneration and required in the <italic>Rd1</italic> photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in <italic>Rd1</italic> mice. Most importantly, genetic ablation of <italic>Bmi1</italic> provided extensive photoreceptor survival and improvement of retinal function in <italic>Rd1</italic> mice, mediated by a decrease in cell cycle markers and regulators independent of p16<sup>Ink4a</sup> and p19<sup>Arf</sup>. These data reveal that Bmi1 controls the cell cycle-related death process, highlighting this pathway as a promising therapeutic target for neuroprotection in retinal dystrophies.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="iso-abbrev">Proc. Natl. Acad. Sci. U.S.A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23359713</article-id><article-id pub-id-type="pmc">3574927</article-id><article-id pub-id-type="publisher-id">201108297</article-id><article-id pub-id-type="doi">10.1073/pnas.1108297110</article-id><article-categories><subj-group subj-group-type="heading"><subject>PNAS Plus</subject></subj-group><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Neuroscience</subject></subj-group></subj-group><series-title>PNAS Plus</series-title></article-categories><title-group><article-title>Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</article-title><alt-title alt-title-type="short">Cell cycle proteins control retinal degeneration</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Zencak</surname><given-names>Dusan</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Schouwey</surname><given-names>Karine</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="fn1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Danian</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref><xref ref-type="author-notes" rid="fn1"><sup>1</sup></xref><xref ref-type="author-notes" rid="fn2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ekström</surname><given-names>Per</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Tanger</surname><given-names>Ellen</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bremner</surname><given-names>Rod</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>van Lohuizen</surname><given-names>Maarten</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Arsenijevic</surname><given-names>Yvan</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="corresp" rid="cor1"><sup>3</sup></xref></contrib><aff id="aff1"><sup>a</sup>Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>, 1004 Lausanne,<country>Switzerland</country>;</aff><aff id="aff2"><sup>b</sup>Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>, Toronto, ON,<country>Canada</country> M5T 2S8;</aff><aff id="aff3"><sup>c</sup>Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>, SE-221 84 Lund,<country>Sweden</country>; and</aff><aff id="aff4"><sup>d</sup>Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>, 1066 CX, Amsterdam,<country>The Netherlands</country></aff></contrib-group><author-notes><corresp id="cor1"><sup>3</sup>To whom correspondence should be addressed. E-mail: <email>yvan.arsenijevic@fa2.ch</email>.</corresp><fn fn-type="edited-by"><p>Edited by Ching-Hwa Sung, Weill Medical College of Cornell University, New York, NY, and accepted by the Editorial Board December 26, 2012 (received for review June 9, 2011)</p></fn><fn fn-type="con"><p>Author contributions: D.Z., K.S., D.C., P.E., R.B., M.v.L., and Y.A. designed research; D.Z., K.S., D.C., P.E., and E.T. performed research; M.v.L. contributed new reagents/analytic tools; D.Z., K.S., D.C., P.E., R.B., M.v.L., and Y.A. analyzed data; and D.Z., K.S., R.B., and Y.A. wrote the paper.</p></fn><fn fn-type="equal" id="fn1"><p><sup>1</sup>K.S. and D.C. contributed equally to this work.</p></fn><fn fn-type="present-address" id="fn2"><p><sup>2</sup>Present address: Department of Ophthalmology, Ophthalmic Laboratory of Molecular Medicine Research Center, and Torsten-Wiesel Research Institute of World Eye Organization, West China Hospital, Sichuan University, Chengdu 610041, China.</p></fn></author-notes><pub-date pub-type="ppub"><day>12</day><month>2</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>28</day><month>1</month><year>2013</year></pub-date><pub-date pub-type="pmc-release"><day>28</day><month>1</month><year>2013</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>110</volume><issue>7</issue><fpage>E593</fpage><lpage>E601</lpage><page-range>E593–E601</page-range><permissions><license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p></license></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="pnas.201108297.pdf"></self-uri><self-uri content-type="author-summary-pdf" xlink:type="simple" xlink:href="pnas.201108297_summary.pdf"></self-uri><abstract id="d34e224"><p>The epigenetic regulator Bmi1 controls proliferation in many organs. Reexpression of cell cycle proteins such as cyclin-dependent kinases (CDKs) is a hallmark of neuronal apoptosis in neurodegenerative diseases. Here we address the potential role of Bmi1 as a key regulator of cell cycle proteins during neuronal apoptosis. We show that several cell cycle proteins are expressed in different models of retinal degeneration and required in the <italic>Rd1</italic> photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in <italic>Rd1</italic> mice. Most importantly, genetic ablation of <italic>Bmi1</italic> provided extensive photoreceptor survival and improvement of retinal function in <italic>Rd1</italic> mice, mediated by a decrease in cell cycle markers and regulators independent of p16<sup>Ink4a</sup> and p19<sup>Arf</sup>. These data reveal that Bmi1 controls the cell cycle-related death process, highlighting this pathway as a promising therapeutic target for neuroprotection in retinal dystrophies.</p></abstract><kwd-group><kwd>blindness</kwd><kwd>neurodegeneration</kwd><kwd>polycomb</kwd></kwd-group><counts><page-count count="9"></page-count></counts><custom-meta-group><custom-meta><meta-name>author-summary</meta-name><meta-value><xref ref-type="other" rid="author-summary"></xref></meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000664 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 000664 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= Pmc
|étape= Corpus
|type= RBID
|clé=
|texte=
}}
| This area was generated with Dilib version V0.6.29. |  |