Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2005-4-27
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
pubmed:status
MEDLINE
pubmed:issn
0378-5866
pubmed:author
pubmed:copyrightInfo
Copyright 2004 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
435-45
pubmed:dateRevised
2009-11-19
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
pubmed:year
2004
pubmed:articleTitle
Distinct capacities of individual E2Fs to induce cell cycle re-entry in postmitotic lens fiber cells of transgenic mice.
pubmed:affiliation
College of Optometry, University of Houston, Houston, Texas, USA.
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