Principle of the Assay: JAK ELISA kit applies the competitive enzyme immunoassay technique utilizing a polyclonal anti-JAK antibody and an JAK-HRP conjugate. The assay sample and buffer are incubated together with JAK-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the JAK concentration since JAK from samples and JAK-HRP conjugate compete for the anti-JAK antibody binding site. Since the number of sites is limited, as more sites are occupied by JAK from the sample, fewer sites are left to bind JAK-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The JAK concentration in each sample is interpolated from this standard curve.
NCBI and Uniprot Product Information
NCBI Description
This gene product is a protein tyrosine kinase involved in a specific subset of cytokine receptor signaling pathways. It has been found to be constituitively 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. [provided by RefSeq, Jul 2008]
Uniprot Description
JAK2: 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.
Protein type: Oncoprotein; Protein kinase, TK; Kinase, protein; EC 2.7.10.2; Protein kinase, tyrosine (non-receptor); TK group; JakA family
Chromosomal Location of Human Ortholog: 9p24
Cellular Component: nucleoplasm; extrinsic to internal side of plasma membrane; nuclear matrix; cytoskeleton; cytoplasm; caveola; nucleus; cytosol; lipid raft
Molecular Function: protein C-terminus binding; histone binding; acetylcholine receptor binding; non-membrane spanning protein tyrosine kinase activity; protein kinase binding; protein kinase activity; interleukin-12 receptor binding; protein binding; growth hormone receptor binding; peptide hormone receptor binding; protein-tyrosine kinase activity; insulin receptor substrate binding; heme binding; phosphoinositide 3-kinase binding; type 1 angiotensin receptor binding; SH2 domain binding; ATP binding; receptor binding
Biological Process: establishment and/or maintenance of chromatin architecture; positive regulation of nitric oxide biosynthetic process; activation of MAPKK activity; tyrosine phosphorylation of Stat3 protein; response to lipopolysaccharide; tyrosine phosphorylation of JAK2 protein; enzyme linked receptor protein signaling pathway; protein amino acid phosphorylation; positive regulation of tyrosine phosphorylation of Stat3 protein; response to antibiotic; regulation of apoptosis; 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 transcription from RNA polymerase II promoter; 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; platelet-derived growth factor receptor signaling pathway; signal transduction; host programmed cell death induced by symbiont; negative regulation of cell proliferation; actin filament polymerization; positive regulation of cell proliferation; cell differentiation; STAT protein nuclear translocation; caspase activation; cell migration; cytokine and chemokine mediated signaling pathway; negative regulation of DNA binding; regulation of cell proliferation; G-protein coupled receptor protein signaling pathway; positive regulation of interleukin-1 beta production; positive regulation of tyrosine phosphorylation of Stat5 protein; regulation of inflammatory response; innate immune 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
Disease: Polycythemia Vera; Myelofibrosis; Budd-chiari Syndrome; Erythrocytosis, Familial, 1; Thrombocythemia 3