a protein kinase of the MAPK family that is potently activated by a variety of environmental stresses, including UV and gamma radiation, ceramides, pro-inflammatory cytokines and, in some instances, by growth factors and GPCR agonists. Substrates include a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2, thus regulating AP-1 transcriptional activity. In T- cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells. Binds to at least four scaffolding proteins, JIP-1, -2, -3 and -4. Activity increased in obesity. Inhibition or mouse knockout increases insulin sensitivity. Part of NFB pathway involved in inflammation and cancer, and signals downstream of Ras, though possibly as an apoptotic negative regulator of growth. Four alternatively-spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, CMGC; Kinase, protein; EC 22.214.171.124; Protein kinase, Ser/Thr (non-receptor); CMGC group; MAPK family; MAPK/JNK subfamily; JNK subfamily
Molecular Function: ATP binding; enzyme binding; histone deacetylase binding; histone deacetylase regulator activity; JUN kinase activity; kinase activity; protein binding; protein serine/threonine kinase activity
Biological Process: JNK cascade; JUN phosphorylation; negative regulation of apoptosis; negative regulation of protein binding; peptidyl-serine phosphorylation; peptidyl-threonine phosphorylation; positive regulation of apoptosis; positive regulation of cyclase activity; positive regulation of protein metabolic process; protein amino acid phosphorylation; regulation of circadian rhythm; regulation of histone deacetylation; regulation of macroautophagy; regulation of protein localization; regulation of transcription factor activity; response to stress; response to UV; 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.