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

Correspondence: Anning LIN, Tel: +773-753-1408; Fax: +773-702-6260; E-mail: alin@huggins.bsd.uchicago.edu

Abstract

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