Volume 15, No 1, Jan 2005

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 15 Issue 1, January 2005: 36-42

REVIEWS

Role of JNK activation in apoptosis: A double-edged sword

Jing LIU, Anning LIN*

Ben May Institute for Cancer Research, The University of Chicago, 5841 S. Maryland Avenue, MC 6027, Chicago, IL 60637, USA Correspondence: Anning LIN(alin@huggins.bsd.uchicago.edu)

JNK is a key regulator of many cellular events, including programmed cell death (apoptosis). In the absence of NF-κB activation, prolonged JNK activation contributes to TNF-α 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.

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