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c-Jun downregulation by HDAC3-dependent transcriptional repression promotes osmotic stress-induced cell apoptosis.

Abstract：

:c-Jun, a major transcription factor in the activating protein 1 (AP-1) family of regulatory proteins, is activated by many physiologic and pathologic stimuli. However, whether c-jun is regulated by epigenetic modification of chromatin structure is not clear. We showed here that c-jun was transcriptionally repressed in response to osmotic stress via a truncated HDAC3 generated by caspase-7-dependent cleavage at aspartic acid 391. The activation of caspase-7, which is independent of cytochrome c release and activation of caspase-9 and caspase-12, depends on activation of caspase-8, which in turn requires MEK2 activity and secretion of FAS ligand. The cell apoptosis induced by the truncated HDAC3 or enhanced by c-Jun deficiency during osmotic stress was suppressed by exogenous expression of c-Jun, indicating that the downregulation of c-Jun by HDAC3-dependent transcriptional repression plays a role in regulating cell survival and apoptosis.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Xia Y,Wang J,Liu TJ,Yung WK,Hunter T,Lu Z

doi

10.1016/j.molcel.2007.01.005

subject

Has Abstract

pub_date

2007-01-26 00:00:00

pages

219-32

issue

2

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(07)00009-3

journal_volume

25

pub_type

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