Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis.
摘要：
Besides its role in , () initiates a cascade. Diverse apoptotic stimuli activate inducible () or (), with the generated nitric (NO) S-nitrosylating , abolishing its and conferring on it the ability to bind to , an E3--ligase with a nuclear signal (). The -protein complex, in turn, translocates to the and mediates ; these processes are blocked by procedures that interfere with -. Nuclear events induced by to kill cells have been obscure. Here we show that nuclear is acetylated at 160 by the /() through direct protein interaction, which in turn stimulates the acetylation and of /. Consequently, downstream targets of /, such as (Refs 10,11,12,13,14,15), are activated and cause . A dominant-negative mutant with the substitution of 160 to (-K160R) prevents activation of /, blocks induction of apoptotic genes and decreases . Our findings reveal a pathway in which NO-induced nuclear mediates through /.
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关键词：
Animals Humans Mice Macrophages, Peritoneal Cell Line Cell Nucleus Acetylation Apoptosis Nitric Oxide Synthase Type II Nitric Oxide
DOI：
10.1038/ncb1747
被引量：
年份：
2008
Nature
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