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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2003-4-2
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-10430607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-10480951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-10545703,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-10555149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-10984511,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-11062132,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-11832206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-11875499,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-12120092,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-12193789,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-12203116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-12209154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-12374983,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-7757980,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-7954799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-8358789,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-8505985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12670866-9020077
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/BAX protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/BCL2L1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0890-9369
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
832-7
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12670866-Apoptosis,
pubmed-meshheading:12670866-Caspase 2,
pubmed-meshheading:12670866-Caspases,
pubmed-meshheading:12670866-Cloning, Molecular,
pubmed-meshheading:12670866-Colorectal Neoplasms,
pubmed-meshheading:12670866-Genes, p53,
pubmed-meshheading:12670866-Humans,
pubmed-meshheading:12670866-Proto-Oncogene Proteins,
pubmed-meshheading:12670866-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:12670866-RNA, Small Interfering,
pubmed-meshheading:12670866-Tumor Cells, Cultured,
pubmed-meshheading:12670866-bcl-2-Associated X Protein,
pubmed-meshheading:12670866-bcl-X Protein
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pubmed:year |
2003
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pubmed:articleTitle |
Bcl-2 constitutively suppresses p53-dependent apoptosis in colorectal cancer cells.
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pubmed:affiliation |
Yorkshire Cancer Research P53 Laboratory, Department of Biology, University of York, York YO10 5DD, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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