UNIPROT #

O60674

PROTEIN NAME

JAK2

SYNONYMS

JAK 2 antibody; JAK-2 antibody; JAK2 antibody; JAK2_HUMAN antibody; Janus Activating Kinase 2 antibody; Janus kinase 2 (a protein tyrosine kinase) antibody; Janus kinase 2 antibody; JTK 10 antibody; JTK10 antibody; kinase Jak2 antibody; OTTHUMP00000043260 antibody; THCYT3 antibody; Tyrosine protein kinase JAK2 antibody; Tyrosine-protein kinase JAK2 antibody

SEQUENCE SIMILARITIES

Belongs to the protein kinase superfamily. Tyr protein kinase family. JAK subfamily.

TISSUE SPECIFICITY

Ubiquitously expressed throughout most tissues.

POST-TRANSLATIONAL MODIFICATION

Autophosphorylated, leading to regulate its activity. Leptin promotes phosphorylation on tyrosine residues, including phosphorylation on Tyr-813 (By similarity). Autophosphorylation on Tyr-119 in response to EPO down-regulates its kinase activity (By similarity). Autophosphorylation on Tyr-868, Tyr-966 and Tyr-972 in response to growth hormone (GH) are required for maximal kinase activity (By similarity). Also phosphorylated by TEC (By similarity). Phosphorylated on tyrosine residues in response to interferon gamma signaling. Phosphorylated on tyrosine residues in response to a signaling cascade that is activated by increased cellular retinol.

SUBCELLULAR LOCATION

Endomembrane system. Nucleus.

FUNCTION

JAK2 (Janus kinase 2) belongs to the emerging family of non-receptor Janus tyrosine kinases, which regulate a spectrum of cellular functions downstream of activated cytokine receptors in the lympho-hematopoietic system. Immunological stimuli, such as interferons and cytokines, induce recruitment of Stat transcription factors to cytokine receptor-associated JAK2. JAK2 then phosphorylates proximal Stat factors, which subsequently dimerize, translocate to the nucleus and bind to cis elements upstream of target gene promoters to regulate transcription. The canonical JAK/Stat pathway is integral to maintaining a normal immune system by stimulating proliferation, differentiation, survival and host resistance to pathogens. Altering JAK/Stat signaling to reduce cytokine induced pro-inflammatory responses represents an attractive target for anti-inflammatory therapies.