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Perspectives
The Two Faces of NF?B in Cell Survival Responses
Bonnie Graham and Spencer B. Gibson
volume 4 | issue 10
october 2005Pages: 1342 - 1345
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Activation of NF?B is controlled by a diverse range of stimuli including growth factors, and apoptotic inducers, but paradoxically these stimuli seem to activate the same NF?B signaling pathways. In particular, growth factors leading to cell survival and DNA damaging agents leading to apoptosis seem to activate the same NF?B signaling pathway. Post-translational modifications of NF?B and surrounding histones give selective targeting of NF?B regulated genes contributing to cell survival or apoptosis. NF?B activation induces death receptor 5 (DR5) expression following DNA damaging agent etoposide treatment but not following growth factor EGF treatment. This differential expression is regulated by the recruitment of histone deacytelasse 1 (HDAC1) to the DR5 gene by NF?B following EGF treatment but not etoposide treatment. In addition, HDAC inhibitors induce NF?B binding to the DR5 gene and DR5 expression, contributing to HDAC inhibitor induced apoptosis. These findings provide a possible model for selective NF?B transcriptional regulation based upon the context of post-translational modifications in surrounding histones on NF?B regulated target genes.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.