rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5-6
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pubmed:dateCreated |
2005-4-27
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pubmed:abstractText |
Inactivation of the retinoblastoma gene in human retinoblasts or mouse lens fiber cells causes inappropriate cell cycle entry, presumably as a consequence of elevated activity of the E2F transcription factors. Although E2Fs are known to be critical regulators of the cell cycle, it is still unclear whether family members E2F3a, E2F4 or E2F5 are individually capable of inducing cell cycle entry in vivo. In this study, we designed experiments to test whether lens-specific expression of these E2F family members would induce postmitotic fiber cells to re-enter the cell cycle.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCNA2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CCNB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ccnb1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin A,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin A2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin B,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin B1,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/E2F Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/E2F3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/E2F4 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/E2F4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/E2F5 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/E2f3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/E2f4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/E2f5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/tumor suppressor protein p73
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pubmed:status |
MEDLINE
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pubmed:issn |
0378-5866
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2004 S. Karger AG, Basel.
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pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
435-45
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15855772-Animals,
pubmed-meshheading:15855772-Apoptosis,
pubmed-meshheading:15855772-Cell Cycle Proteins,
pubmed-meshheading:15855772-Cyclin A,
pubmed-meshheading:15855772-Cyclin A2,
pubmed-meshheading:15855772-Cyclin B,
pubmed-meshheading:15855772-Cyclin B1,
pubmed-meshheading:15855772-DNA-Binding Proteins,
pubmed-meshheading:15855772-E2F Transcription Factors,
pubmed-meshheading:15855772-E2F3 Transcription Factor,
pubmed-meshheading:15855772-E2F4 Transcription Factor,
pubmed-meshheading:15855772-E2F5 Transcription Factor,
pubmed-meshheading:15855772-Eye Abnormalities,
pubmed-meshheading:15855772-Gene Expression Regulation, Developmental,
pubmed-meshheading:15855772-Genes, Tumor Suppressor,
pubmed-meshheading:15855772-Humans,
pubmed-meshheading:15855772-Lens, Crystalline,
pubmed-meshheading:15855772-Mice,
pubmed-meshheading:15855772-Mice, Transgenic,
pubmed-meshheading:15855772-Nuclear Proteins,
pubmed-meshheading:15855772-Transcription Factors,
pubmed-meshheading:15855772-Tumor Suppressor Protein p53,
pubmed-meshheading:15855772-Tumor Suppressor Proteins
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pubmed:year |
2004
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pubmed:articleTitle |
Distinct capacities of individual E2Fs to induce cell cycle re-entry in postmitotic lens fiber cells of transgenic mice.
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pubmed:affiliation |
College of Optometry, University of Houston, Houston, Texas, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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