Jiang, M. and Milner, J. (2003) Bcl-2 constitutively suppresses p53-dependent apoptosis in colorectal cancer cells. Genes and Development, 17 (7). pp. 832-837. ISSN 0890-9369Full text not available from this repository.
To dissect apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence Bcl-2 and Bcl-xLin 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.
|Academic Units:||The University of York > Biology (York)|
|Depositing User:||York RAE Import|
|Date Deposited:||27 May 2009 13:41|
|Last Modified:||27 May 2009 13:41|
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