Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities

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Diverse stimuli initiate the activation of apoptotic signaling pathways that often causes nuclear DNA fragmentation. Here, we report a new antiapoptotic protein, a caspase-activated DNase (CAD) inhibitor that interacts with ASK1 (CIIA). CIIA, by binding to apoptosis signal-regulating kinase 1 (ASKI), inhibits oligomerization-induced ASK1 activation. CIIA also associates with CAD and inhibits the nuclease activity of CAD without affecting caspase-3-mediated ICAD cleavage. Overexpressed CIIA reduces H2O2- and tumor necrosis factor-a-induced apoptosis. CIIA antisense oligonucleotides, which abolish expression of endogenous CIIA in murine L929 cells, block the inhibitory effect of CIA on ASK1 activation, deoxyribonucleic acid fragmentation, and apoptosis. These findings suggest that CIIA is an endogenous antagonist of both ASK1 -.and CAD-mediated signaling.
Publisher
ROCKEFELLER UNIV PRESS
Issue Date
2003-10
Language
English
Article Type
Article
Keywords

SIGNAL-REGULATING KINASE-1; DNA FRAGMENTATION FACTOR; CASPASE-ACTIVATED DNASE; N-TERMINAL KINASE; MAMMALIAN-CELLS; MAP KINASES; APOPTOSIS; INHIBITOR; STRESS; TRANSDUCTION

Citation

JOURNAL OF CELL BIOLOGY, v.163, pp.71 - 81

ISSN
0021-9525
DOI
10.1083/jcb.200303003
URI
http://hdl.handle.net/10203/82994
Appears in Collection
BS-Journal Papers(저널논문)
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