Product Name: JAK2 (1004-1011) pY1007+pY1008
Product Number: PE-04AVO01
Size:      $US
Peptide Name: JAK2 (1004-1011) pY1007+pY1008

Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T loop region between subdomains VII and VIII. Y1007 and Y1008 phosphorylation stimulate phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: DKE(pY)(pY)KVK

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Modifications Other: Phosphorylated
Storage Conditions: -20°C

Scientific Background: JAK2 is a protein-tyrosine kinase of the TK group and JakA family. It is a non-receptor kinase involved in the regulation of various cellular processes, including cell cycle progression, development, differentiation, and histone modifications. Additionally, JAK2 plays a critical role in the signalling events of both innate and adaptive immunity as well as erythropoiesis. JAK2 can pair with type I receptors to mediate signalling for GHR (growth hormone), PRLR (prolactin), (LEPR) leptin, EPOR (erythropoietin), and THPO (thrombopoietin). JAK2 can also pair with type II receptors to mediate the effects of IFN-alpha, IFN-beta, IFN-gamma, and various interleukins. It is activated by phosphorylation at Y613, and Y972, and Y1008. JAK2 signalling has been implicated in in a wide range of human hematologic malignancies, and this is typically accompanied by the over-activation of the STAT5 transcription factor, which is a substrate. Polycythemia vera, thrombocythemia, and myelofibrosis are classified as clonal myeloproliferative diseases that arise from a multipotent progenitor cell type. These often rare diseases are characterized by excess production of abnormal cells, displacing healthy cells. JAK2 is a known oncoprotein (OP). Cancer-related mutations in human tumours point to a gain of function of the protein kinase. A high percentage of patients with these myeloproliferative diseases have a dominant gain-of-function substitution mutation, V617F, in the JAK2 gene sequence. For example, the V617F mutation was observed in 40 of 45 polycythemia vera patients. The mutation was observed to cause constitutive tyrosine phosphotransferase activity that promoted erythrocytosis in a mouse model.