Product Name: JAK2Selectide
Product Number: PE-01BHR90
Size: 200 µg      Price:45.00
1 mg      $US91.00
5 mg      214.00
Peptide Name: JAK2Selectide

Product Use: For assaying the phosphotransferase activity of Janus protein-tyrosine kinase 2 (UniProt ID O60674).

Peptide Production Method: Solid-phase peptide synthesis

Peptide Sequence: KKRGAIDDYVKVQI

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Molecular Mass Calculated: 1807.09 Da

Peptide Purity Percent after Synthesis and Purification: >90

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: JAK2

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.