a protein kinase of the MAPK family that is potently activated by a variety of environmental stresses including UV radiation. Phosphorylates specific transcription factors such as c-Jun and ATF2, mediating immediate-early gene expression. Closely related to JNK1. Both are involved in UV radiation induced apoptosis. Blocks the ubiquitination of tumor suppressor p53, and thus it increases the stability of p53 in nonstressed cells. JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells in the mouse. Four alternatively-spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Protein kinase, CMGC; EC 126.96.36.199; Protein kinase, Ser/Thr (non-receptor); CMGC group; MAPK family; MAPK/JNK subfamily; JNK subfamily
Molecular Function: ATP binding; caspase activator activity; JUN kinase activity; mitogen-activated protein kinase kinase kinase binding; protein binding; transcription factor binding
Biological Process: caspase activation; central nervous system development; JNK cascade; JUN phosphorylation; neurite development; positive regulation of chemokine production; positive regulation of nitric oxide biosynthetic process; positive regulation of nitric-oxide synthase biosynthetic process; positive regulation of prostaglandin biosynthetic process; positive regulation of prostaglandin secretion; positive regulation of protein amino acid phosphorylation; positive regulation of transcription, DNA-dependent; protein amino acid phosphorylation; protein targeting to mitochondrion; regulation of circadian rhythm; regulation of JNK cascade; regulation of protein ubiquitination; regulation of transcription factor activity; release of cytochrome c from mitochondria; response to amine stimulus; response to cadmium ion; response to drug; response to mechanical stimulus; response to stress; response to toxin; rhythmic process
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.