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| pubmed-article:12670866 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12670866 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:12670866 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
| pubmed-article:12670866 | lifeskim:mentions | umls-concept:C1527249 | lld:lifeskim |
| pubmed-article:12670866 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:12670866 | pubmed:dateCreated | 2003-4-2 | lld:pubmed |
| pubmed-article:12670866 | pubmed:abstractText | To dissect apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence Bcl-2 and Bcl-x(L) in isogenic clones of p53+/+ and p53-/- cells, and of Bax+/- and Bax-/- cells. We identify a novel proapoptotic function of p53 that does not require activation by genotoxic agents and that appears to be constitutively suppressed by Bcl-2. Silencing of Bcl-2 induced massive p53-dependent apoptosis. The "Bcl-2/p53 axis" requires Bax and caspase 2 as essential apoptotic mediators. This newly discovered Bcl-2/p53 functional interface represents a key regulator of apoptosis which can be activated by targeting Bcl-2 in colorectal carcinoma cells. | lld:pubmed |
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| pubmed-article:12670866 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12670866 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12670866 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12670866 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:12670866 | pubmed:issn | 0890-9369 | lld:pubmed |
| pubmed-article:12670866 | pubmed:author | pubmed-author:MingJiangJ | lld:pubmed |
| pubmed-article:12670866 | pubmed:author | pubmed-author:MilnerJoJ | lld:pubmed |
| pubmed-article:12670866 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12670866 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12670866 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:12670866 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12670866 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12670866 | pubmed:pagination | 832-7 | lld:pubmed |
| pubmed-article:12670866 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12670866 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12670866 | pubmed:articleTitle | Bcl-2 constitutively suppresses p53-dependent apoptosis in colorectal cancer cells. | lld:pubmed |
| pubmed-article:12670866 | pubmed:affiliation | Yorkshire Cancer Research P53 Laboratory, Department of Biology, University of York, York YO10 5DD, UK. | lld:pubmed |
| pubmed-article:12670866 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12670866 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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