Abstract
JNK 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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Apoptosis
-
Carrier Proteins / metabolism
-
Cell Line
-
Enzyme Activation
-
Hematopoietic Stem Cells / cytology
-
Humans
-
Interleukin-3 / metabolism
-
JNK Mitogen-Activated Protein Kinases / metabolism*
-
MAP Kinase Kinase 4
-
Mice
-
Mitogen-Activated Protein Kinase Kinases / metabolism*
-
Models, Biological
-
NF-kappa B / metabolism
-
Phosphorylation
-
Proto-Oncogene Proteins c-bcl-2 / metabolism
-
Signal Transduction
-
Ultraviolet Rays
-
bcl-Associated Death Protein
Substances
-
BAD protein, human
-
Bad protein, mouse
-
Carrier Proteins
-
Interleukin-3
-
NF-kappa B
-
Proto-Oncogene Proteins c-bcl-2
-
bcl-Associated Death Protein
-
JNK Mitogen-Activated Protein Kinases
-
MAP Kinase Kinase 4
-
Mitogen-Activated Protein Kinase Kinases