摘要
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, depend- ing on cell type, nature of the death stimulus, duration of its activation and the activity of other signaling pathways.
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, depend- ing on cell type, nature of the death stimulus, duration of its activation and the activity of other signaling pathways.
