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

628Citations
Citations of this article
422Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

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.

Author supplied keywords

Cite

CITATION STYLE

APA

Liu, J., & Lin, A. (2005). Role of JNK activation in apoptosis: A double-edged sword. Cell Research. https://doi.org/10.1038/sj.cr.7290262

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free