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Role of JNK activation in apoptosis: a double-edged sword Liu J; Lin ACell Res 2005[Jan]; 15 (1): 36-42JNK is a key regulator of many cellular events, including programmed cell death (apoptosis). In the absence of NF-kB activation, prolonged JNK activation contributes to TNF-a 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.|Animals[MESH]|Apoptosis[MESH]|Carrier Proteins/metabolism[MESH]|Cell Line[MESH]|Enzyme Activation[MESH]|Hematopoietic Stem Cells/cytology[MESH]|Humans[MESH]|Interleukin-3/metabolism[MESH]|JNK Mitogen-Activated Protein Kinases/*metabolism[MESH]|MAP Kinase Kinase 4[MESH]|Mice[MESH]|Mitogen-Activated Protein Kinase Kinases/*metabolism[MESH]|Models, Biological[MESH]|NF-kappa B/metabolism[MESH]|Phosphorylation[MESH]|Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]|Signal Transduction[MESH]|Ultraviolet Rays[MESH]|bcl-Associated Death Protein[MESH] |
