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Cell Res. 2005 Jan;15(1):36-42.

Role of JNK activation in apoptosis: a double-edged sword.

Author information

1
Ben May Institute for Cancer Research, The University of Chicago, 5841 S. Maryland Avenue, MC 6027, Chicago, IL 60637, USA.

Abstract

JNK is a key regulator of many cellular events, including programmed cell death (apoptosis). In the absence of NF-kB activation, prolonged JNK activation contributes to TNF-a induced apoptosis. JNK is also essential for UV induced apoptosis. However, recent studies reveal that JNK can suppress apoptosis in IL-3-dependent hematopoietic cells via phosphorylation of the proapoptotic Bcl-2 family protein BAD. Thus, JNK has pro- or antiapoptotic functions, depending on cell type, nature of the death stimulus, duration of its activation and the activity of other signaling pathways.

PMID:
15686625
DOI:
10.1038/sj.cr.7290262
[Indexed for MEDLINE]
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