a non-receptor tyrosine-kinase involved in a specific subset of cytokine receptor signaling pathways, including IL-3, -5 and GM-CSF. Interacts with IL23R, SKB1 and STAM2. It has been found to be constitutively associated with the prolactin receptor and is required for responses to gamma interferon. Mice that do not express an active protein for this gene exhibit embryonic lethality associated with the absence of definitive erythropoiesis. Fusion of Jak2 to TEL1 (ETV6) by t(9;12)(p24;p13) causes myeloproliferative disease in humans and mouse models. The Jak inhibitor AG490 inhibits constitutive Jak2 phosphorylation and causes apoptosis in cells from breast cancer and relapsing acute lymphoblastic leukemia. A single activating mutation is associated with several hematological malignancies. Inhibitor: AG490. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, TK; EC 184.108.40.206; Protein kinase, tyrosine (non-receptor); Kinase, protein; TK group; JakA family
Molecular Function: protein C-terminus binding; histone binding; non-membrane spanning protein tyrosine kinase activity; acetylcholine receptor binding; protein kinase binding; interleukin-12 receptor binding; protein kinase activity; protein binding; growth hormone receptor binding; peptide hormone receptor binding; insulin receptor substrate binding; protein-tyrosine kinase activity; heme binding; phosphoinositide 3-kinase binding; type 1 angiotensin receptor binding; SH2 domain binding; ATP binding; receptor binding
Biological Process: positive regulation of nitric oxide biosynthetic process; activation of MAPKK activity; positive regulation of apoptosis; tyrosine phosphorylation of Stat3 protein; response to lipopolysaccharide; tyrosine phosphorylation of JAK2 protein; protein amino acid phosphorylation; enzyme linked receptor protein signaling pathway; positive regulation of tyrosine phosphorylation of Stat3 protein; response to antibiotic; elevation of cytosolic calcium ion concentration; tumor necrosis factor-mediated signaling pathway; erythrocyte differentiation; mesoderm development; negative regulation of neuron apoptosis; positive regulation of cell activation; positive regulation of DNA binding; positive regulation of protein import into nucleus, translocation; axon regeneration; positive regulation of insulin secretion; JAK-STAT cascade; positive regulation of tumor necrosis factor production; tyrosine phosphorylation of Stat5 protein; positive regulation of phosphoinositide 3-kinase cascade; tyrosine phosphorylation of STAT protein; positive regulation of peptidyl-tyrosine phosphorylation; response to hydroperoxide; mineralocorticoid receptor signaling pathway; tyrosine phosphorylation of Stat1 protein; positive regulation of transcription factor activity; positive regulation of cell differentiation; positive regulation of nitric-oxide synthase biosynthetic process; positive regulation of phosphoprotein phosphatase activity; peptidyl-tyrosine phosphorylation; hormone-mediated signaling; negative regulation of heart contraction; apoptosis; protein amino acid autophosphorylation; protein kinase cascade; platelet-derived growth factor receptor signaling pathway; signal transduction; negative regulation of cell proliferation; actin filament polymerization; positive regulation of cell proliferation; cell differentiation; STAT protein nuclear translocation; caspase activation; cytokine and chemokine mediated signaling pathway; negative regulation of DNA binding; positive regulation of interleukin-1 beta production; G-protein coupled receptor protein signaling pathway; positive regulation of tyrosine phosphorylation of Stat5 protein; regulation of inflammatory response; negative regulation of cell-cell adhesion; blood coagulation; cell motility; induction of apoptosis by oxidative stress; positive regulation of inflammatory response; positive regulation of cell migration
SS: 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.