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TAF II 105 mediates activation of anti‐apoptotic genes by NF‐κB
Author(s) -
YamitHezi Ayala,
Dikstein Rivka
Publication year - 1998
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/17.17.5161
Subject(s) - biology , nfkb1 , gene , kappa , apoptosis , genetics , nf κb , cancer research , microbiology and biotechnology , transcription factor , linguistics , philosophy
The transcription factor NF‐κB is important for expression of genes involved in immune responses, viral infections, cytokine signaling and stress. In addition NF‐κB plays a crucial role in protecting cells from TNF‐α‐induced apoptotic stimuli, presumably by activating anti‐apoptotic genes. Here we report that the sub‐stoichiometric TFIID subunit TAF II 105 is essential for activation of anti‐apoptotic genes in response to TNF‐α, serving as a transcriptional coactivator for NF‐κB. The putative coactivator domain of TAF II 105 interacts with the activation domain of the p65/RelA member of the NF‐κB family, and further stimulates p65‐induced transcription in human 293 cells. Moreover, inhibition of TAF II 105 activity by overexpression of a dominant negative mutant of TAF II 105 decreased NF‐κB transcriptional activity and severely reduced cell survival in response to TNF‐α. Similarly, expression of anti‐sense TAF II 105 RNA sensitized the cells to TNF‐α cytotoxicity. These results suggest that TAF II 105 is involved in activation of anti‐apoptotic genes by NF‐κB.