a protein kinase of the MAPK family that is potently activated by a variety of environmental stress and pro-inflammatory cytokines. Brain-selective JNK isoform. A pro-apoptotic protein and potential tumor suppressor. Phosphorylates a number of transcription factors including c-Jun, ATF2 and ELK1. Required for stress-induced neuronal apoptosis and the pathogenesis of glutamate excitotoxicity. CDK5 can phosphorylate and inhibit the activity of this kinase, which may be important in preventing neuronal apoptosis. Binds to at least four scaffolding proteins, JIP-1, -2, -3 and -4. Interacts with HDAC9. Expression lost in brain tumors. May function in neuronal cell death from injury and neurodegeneration, for which inhibitors are being developed. Two alternatively spliced transcript variants have been reported. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 126.96.36.199; Protein kinase, CMGC; CMGC group; MAPK family; JNK subfamily; MAPK/JNK subfamily
Chromosomal Location of Human Ortholog: 4q22.1-q23
Molecular Function: ATP binding; JUN kinase activity; MAP kinase kinase activity; protein binding
Biological Process: activation of MAPK activity; JNK cascade; JUN phosphorylation; protein amino acid phosphorylation; regulation of circadian rhythm; regulation of transcription factor activity; response to light stimulus; rhythmic process; signal transduction
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.