| pubmed-article:11404460 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11404460 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11404460 | lifeskim:mentions | umls-concept:C0034786 | lld:lifeskim |
| pubmed-article:11404460 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:11404460 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:11404460 | pubmed:dateCreated | 2001-6-20 | lld:pubmed |
| pubmed-article:11404460 | pubmed:abstractText | Whereas several apoptosis-related proteins have been linked to the antiapoptotic effects of Akt serine-threonine kinase, the search continues to explain the Akt signaling role in promoting cell survival via antiapoptotic effects. Here, we demonstrate that Akt phosphorylates the androgen receptor (AR) at Ser-210 and Ser-790. A mutation at AR Ser-210 results in the reversal of Akt-mediated suppression of AR transactivation. Activation of the phosphatidylinositol-3-OH kinase/Akt pathway results in the suppression of AR target genes, such as p21, and the decrease of androgen/AR-mediated apoptosis, which may involve the inhibition of interaction between AR and AR coregulators. Together, these findings provide a molecular basis for cross-talk between two signaling pathways at the level of Akt and AR-AR coregulators that may help us to better understand the roles of Akt in the androgen/AR-mediated apoptosis. | lld:pubmed |
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| pubmed-article:11404460 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11404460 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11404460 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11404460 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11404460 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11404460 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11404460 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:11404460 | pubmed:author | pubmed-author:ChangCC | lld:pubmed |
| pubmed-article:11404460 | pubmed:author | pubmed-author:YehSS | lld:pubmed |
| pubmed-article:11404460 | pubmed:author | pubmed-author:LioH HHH | lld:pubmed |
| pubmed-article:11404460 | pubmed:author | pubmed-author:KangH YHY | lld:pubmed |
| pubmed-article:11404460 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11404460 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:11404460 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:11404460 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11404460 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11404460 | pubmed:pagination | 7200-5 | lld:pubmed |
| pubmed-article:11404460 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:11404460 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11404460 | pubmed:articleTitle | Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor. | lld:pubmed |
| pubmed-article:11404460 | pubmed:affiliation | George Whipple Laboratory for Cancer Research, Department of Pathology, and The Cancer Center, University of Rochester, Rochester, NY 14642, USA. | lld:pubmed |
