| pubmed-article:19457859 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1416657 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C0007586 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1414223 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C0215398 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C0439851 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1552596 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1947931 | lld:lifeskim |
| pubmed-article:19457859 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:19457859 | pubmed:issue | 31 | lld:pubmed |
| pubmed-article:19457859 | pubmed:dateCreated | 2009-7-27 | lld:pubmed |
| pubmed-article:19457859 | pubmed:abstractText | Differentiation of erythroid cells requires precise control over the cell cycle to regulate the balance between cell proliferation and differentiation. The zinc finger transcription factor, erythroid Krüppel-like factor (EKLF/KLF1), is essential for proper erythroid cell differentiation and regulates many erythroid genes. Here we show that loss of EKLF leads to aberrant entry into S-phase of the cell cycle during both primitive and definitive erythropoiesis. This cell cycle defect was associated with a significant reduction in the expression levels of E2f2 and E2f4, key factors necessary for the induction of S-phase gene expression and erythropoiesis. We found and validated novel intronic enhancers in both the E2f2 and E2f4 genes, which contain conserved CACC, GATA, and E-BOX elements. The E2f2 enhancer was occupied by EKLF in vivo. Furthermore, we were able to partially restore cell cycle dynamics in EKLF(-/-) fetal liver upon additional genetic depletion of Rb, establishing a genetic causal link between reduced E2f2 and the EKLF cell cycle defect. Finally, we propose direct regulation of the E2f2 enhancer is a generic mechanism by which many KLFs regulate proliferation and differentiation. | lld:pubmed |
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| pubmed-article:19457859 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19457859 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19457859 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19457859 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19457859 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19457859 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19457859 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19457859 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:19457859 | pubmed:author | pubmed-author:KeysJanelle... | lld:pubmed |
| pubmed-article:19457859 | pubmed:author | pubmed-author:PerkinsAndrew... | lld:pubmed |
| pubmed-article:19457859 | pubmed:author | pubmed-author:HumbertPatric... | lld:pubmed |
| pubmed-article:19457859 | pubmed:author | pubmed-author:TallackMichae... | lld:pubmed |
| pubmed-article:19457859 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19457859 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:19457859 | pubmed:volume | 284 | lld:pubmed |
| pubmed-article:19457859 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19457859 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19457859 | pubmed:pagination | 20966-74 | lld:pubmed |
| pubmed-article:19457859 | pubmed:dateRevised | 2010-9-27 | lld:pubmed |
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