| pubmed-article:19917671 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1705627 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C0140278 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1366536 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1158770 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1413181 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1425420 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1549879 | lld:lifeskim |
| pubmed-article:19917671 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:19917671 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19917671 | pubmed:dateCreated | 2010-3-2 | lld:pubmed |
| pubmed-article:19917671 | pubmed:abstractText | Although the role of the classic retinoic acid (RA)-induced genomic pathway in cancer cell differentiation is well recognized, the underlying mechanisms remain to be dissected. Retinoic acid receptor alpha (RARalpha) is a transcription factor activated by RA, and its serine 77 (RARalphaS77) is the main residue phosphorylated by the cyclin-dependent kinase (CDK)-activating kinase (CAK) complex. We report here that in both human myeloid leukemia and mouse embryonic teratocarcinoma stem cells, either RA-suppressed CAK phosphorylation of RARalpha or mutation of RARalphaS77 to alanine (RARalphaS77A) coordinates CAK-dependent G(1) arrest with cancer cell differentiation by transactivating RA-target genes. Both hypophosphorylated RARalpha and RARalphaS77A reduce binding to retinoic acid-responsive elements (RARE) in the promoters of RA-target genes while stimulating gene transcription. The enhanced transactivation and reduced RARalpha-chromatin interaction are accompanied by RARalpha dissociation from the transcriptional repressor N-CoR and are association with the coactivator NCoA-3. Such effects of decreased CAK phosphorylation of RARalphaS77 on mediating RA-dependent transcriptional control of cancer cell differentiation are examined correspondingly in both RA-resistant myeloid leukemia and embryonic teratocarcinoma stem RARalpha(-/-) cells. These studies demonstrate, for the first time, that RA couples G(1) arrest to transcriptional control of cancer cell differentiation by suppressing CAK phosphorylation of RARalpha to release transcriptional repression.-Wang, A., Alimova, I. N., Luo, P. Jong, A., Triche, T. J., Wu, L. Loss of CAK phosphorylation of RARalpha mediates transcriptional control of retinoid-induced cancer cell differentiation. | lld:pubmed |
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| pubmed-article:19917671 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19917671 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19917671 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19917671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19917671 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19917671 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19917671 | pubmed:issn | 1530-6860 | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:TricheTimothy... | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:JongAmbroseA | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:AlimovaIrina... | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:WuLingtaoL | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:WangAnxunA | lld:pubmed |
| pubmed-article:19917671 | pubmed:author | pubmed-author:LuoPeihuaP | lld:pubmed |
| pubmed-article:19917671 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19917671 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:19917671 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19917671 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19917671 | pubmed:pagination | 833-43 | lld:pubmed |
| pubmed-article:19917671 | pubmed:dateRevised | 2011-7-25 | lld:pubmed |
| pubmed-article:19917671 | pubmed:meshHeading | pubmed-meshheading:19917671... | lld:pubmed |
| pubmed-article:19917671 | pubmed:meshHeading | pubmed-meshheading:19917671... | lld:pubmed |
| pubmed-article:19917671 | pubmed:meshHeading | pubmed-meshheading:19917671... | lld:pubmed |
| pubmed-article:19917671 | pubmed:meshHeading | pubmed-meshheading:19917671... | lld:pubmed |
