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| pubmed-article:16682214 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:16682214 | lifeskim:mentions | umls-concept:C0006141 | lld:lifeskim |
| pubmed-article:16682214 | lifeskim:mentions | umls-concept:C1655731 | lld:lifeskim |
| pubmed-article:16682214 | lifeskim:mentions | umls-concept:C0597304 | lld:lifeskim |
| pubmed-article:16682214 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16682214 | pubmed:dateCreated | 2006-6-5 | lld:pubmed |
| pubmed-article:16682214 | pubmed:abstractText | 14-3-3sigma is an epithelial marker whose expression is induced by DNA damage through a p53-dependent pathway. 14-3-3sigma functions sequesters cyclin B1-CDC2 complexes outside the nucleus and thereby contributes to a G2 arrest. Down-regulation or lack of 14-3-3sigma is a frequent event in breast and prostate cancers. Epigenetic silencing by CpG methylation, p53 inactivation, and proteasome-dependent proteolysis leads to loss of 14-3-3sigma. Hypermethylation of the 14-3-3sigma gene is often observed in precancerous lesions and likely to be causally linked to the onset of cancer. Proteolytic inactivation of 14-3-3sigma has been recently found in breast and prostate cancers. In breast cancer, the estrogen-responsive E3 ubiquitin ligase Efp specifically targets 14-3-3sigma for degradation. The E2 ubiquitin conjugating enzyme UBC8 and Efp also mediates ISG15 modification of 14-3-3sigma. Detection of 14-3-3sigma inactivation on the protein or DNA methylation level may be used for cancer prognosis. Furthermore, 14-3-3sigma may be a potential therapeutic target in breast and prostate cancer. | lld:pubmed |
| pubmed-article:16682214 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16682214 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16682214 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16682214 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16682214 | pubmed:issn | 1044-579X | lld:pubmed |
| pubmed-article:16682214 | pubmed:author | pubmed-author:InoueSatoshiS | lld:pubmed |
| pubmed-article:16682214 | pubmed:author | pubmed-author:Horie-InoueKu... | lld:pubmed |
| pubmed-article:16682214 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16682214 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:16682214 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16682214 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16682214 | pubmed:pagination | 235-9 | lld:pubmed |
| pubmed-article:16682214 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:16682214 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16682214 | pubmed:articleTitle | Epigenetic and proteolytic inactivation of 14-3-3sigma in breast and prostate cancers. | lld:pubmed |
| pubmed-article:16682214 | pubmed:affiliation | Research Center for Genomic Medicine and Department of Molecular Biology, Saitama Medical School, Hidaka-shi, Japan. | lld:pubmed |
| pubmed-article:16682214 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16682214 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:16682214 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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