Product Name: JAK1 (1031-1038) pY1034 + pY1035
Product Number: PE-04AVM01
Size:      $US
Peptide Name: JAK1 (1031-1038) pY1034 + pY1035

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. Y1034 and Y1035 phosphorylation stimulate phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: DKE(pY)(pY)TVK

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

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

Scientific Background: JAK1 is a protein-tyrosine kinase of the TK group and JakA family. It is a non-receptor kinase that functions in the IFN-alpha/beta/gamma intracellular signal pathway. JAK1 has also been shown to interact with the interleukin-2 (IL-2) receptor. The JAK1 protein is typically membrane-associated and is widely expressed across different tissues. JAK1 also functions upstream of STAT transcription factors, specifically STAT3, acting to activate the proteins and promote gene transcription. Phosphorylation of Y940 inhibits phosphotransferase activity. JAK1 may be an oncoprotein (OP). Abnormal activity of STAT3 is implicated in the oncogenesis of several cancer types, including colorectal cancer and non-small cell lung cancer. JAK1 has been implicated in promoting the survival, invasion, and migration of colorectal cancer and non-small cell lung cancer cells due to over activation of STAT transcription factors resulting in the aberrant expression of certain downstream genes, such as Bcl-2, p21, p27, E-cadherin, VEGF, and MMPs. In addition, somatic mutations in the JAK1 gene have been observed in patients with acute myeloid leukemia (AML), including both T478S and V623A substitution mutations. The mutant JAK1 proteins displayed significantly enhanced activation of downstream STAT1 in response to type 1 interferon treatment, as well as increased activation of multiple dowstream intracellular signalling pathways. Truncating mutations of JAK1 have been observed in several cancer types, with 68% of the specimens coming from gynecologic cancers. Cancer cells with mutant truncated JAK1 protein are defective in IFN-gamma induced expression of LMP2 and TAP1, which inhibits the presentation of tumour antigens to be recognized by the immune system. Therefore, these truncating mutations are hypothesized to promote the ability of tumour cells to evade the immune system, enabling tumour survival.