pubmed-article:17923680 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C0014762 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C0035335 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C0007586 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C1414223 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C1254042 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C0243067 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C1880287 | lld:lifeskim |
pubmed-article:17923680 | lifeskim:mentions | umls-concept:C0456148 | lld:lifeskim |
pubmed-article:17923680 | pubmed:issue | 24 | lld:pubmed |
pubmed-article:17923680 | pubmed:dateCreated | 2007-11-27 | lld:pubmed |
pubmed-article:17923680 | pubmed:abstractText | By assessing the contribution of deregulated E2F activity to erythroid defects in Rb null mice, we have identified E2f-2 as being upregulated in end-stage red cells, where we show it is the major pRb-associated E2f and the predominant E2f detected at key target gene promoters. Consistent with its expression pattern, E2f-2 loss restored terminal erythroid maturation to Rb null red cells, including the ability to undergo enucleation. Deletion of E2f-2 also extended the life span of Rb null mice despite persistent defects in placental development, indicating that deregulated E2f-2 activity in differentiating erythroblasts contributes to the premature lethality of Rb null mice. We show that the aberrant entry of Rb null erythroblasts into S phase at times in differentiation when wild-type erythroblasts are exiting the cell cycle is inhibited by E2f-2 deletion. E2f-2 loss induced cell cycle arrest in both wild-type and Rb null erythroblasts and was associated with increased DNA double-strand breaks. These results implicate deregulated E2f-2 in the cell cycle defects observed in Rb null erythroblasts and reveal a novel role for E2f-2 during terminal red blood cell differentiation. The identification of a tissue-restricted role for E2f-2 in erythropoiesis highlights the nonredundant nature of E2f transcription factor activities in cell growth and differentiation. | lld:pubmed |
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pubmed-article:17923680 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17923680 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17923680 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17923680 | pubmed:month | Dec | lld:pubmed |
pubmed-article:17923680 | pubmed:issn | 1098-5549 | lld:pubmed |
pubmed-article:17923680 | pubmed:author | pubmed-author:DirlamAlexand... | lld:pubmed |
pubmed-article:17923680 | pubmed:author | pubmed-author:SpikeBenjamin... | lld:pubmed |
pubmed-article:17923680 | pubmed:author | pubmed-author:MacleodKay... | lld:pubmed |
pubmed-article:17923680 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17923680 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:17923680 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17923680 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17923680 | pubmed:pagination | 8713-28 | lld:pubmed |
pubmed-article:17923680 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17923680 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17923680 | pubmed:articleTitle | Deregulated E2f-2 underlies cell cycle and maturation defects in retinoblastoma null erythroblasts. | lld:pubmed |
pubmed-article:17923680 | pubmed:affiliation | Ben May Department for Cancer Research, Gordon Center for Integrative Sciences, The University of Chicago, 929 East 57th Street, Chicago, IL 60637, USA. | lld:pubmed |
pubmed-article:17923680 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17923680 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:17923680 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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