JAK1 Recombinant Rabbit Monoclonal Antibody [JM75-03] (ET1705-84)

UNIPROT #

P23458

PROTEIN NAME

JAK1

SYNONYMS

JAK 1 antibody;JAK 1A antibody;JAK 1B antibody;JAK-1 antibody;JAK1 antibody;JAK1_HUMAN antibody;JAK1A antibody;JAK1B antibody;Janus kinase 1 (a protein tyrosine kinase) antibody;Janus kinase 1 antibody;JTK3 antibody;Tyrosine protein kinase JAK 1 antibody;Tyrosine protein kinase JAK1 antibody;Tyrosine-protein kinase JAK1 antibody

SEQUENCE SIMILARITIES

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

TISSUE SPECIFICITY

Expressed at higher levels in primary colon tumors than in normal colon tissue. The expression level in metastatic colon tumors is comparable to the expression level in normal colon tissue.

POST-TRANSLATIONAL MODIFICATION

Autophosphorylated. Phosphorylated on tyrosine residues in response to interferon gamma signaling. Dephosphorylation of Tyr-1034 and Tyr-1035 by PTPN2 negatively regulates cytokine-mediated signaling.; Ubiquitinated by RNF125; leading to its degradation by the proteasome.

SUBCELLULAR LOCATION

Endomembrane system.

FUNCTION

JAK1 (Janus kinase 1) belongs to the 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 JAK1. JAK1 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. Upon ligand binding, JAK1 undergoes tyrosine phosphorylation and catalytic activation in an interdependent manner. Phosphorylation of tyrosine residues at position 1022 and 1023 is believed to function in the activation of catalytic events. 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.