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.
CITATION STYLE
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
Mendeley helps you to discover research relevant for your work.