Product Name: KDR (1051-1057) pY1054
Product Number: PE-04AGM99
Size: | 200 µg | | Price: | 47.00 |
| 1 mg | | $US | 94.00 |
| 5 mg | | | 206.00 |
Peptide Name: KDR (1051-1057) pY1054
Product Use: Services as a blocking peptide for use with the VEGFR2-pY1054 rabbit polyclonal antibody (Cat. No.: AB-PK852) that is also available from Kinexus. This phosphopeptide may also 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 between subdomains VII and VIII. Y1054 phosphorylation stimulates phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: RDI-pY-KDP
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: βAla-Cys
Scientific Background: VEGFR2 (KDR, FLK1) is a protein-tyrosine kinase of the TK group and VEGFR (vascular endothelial growth factor receptor) family. It is a receptor kinase that binds VEGFA, VEGFC, and VEGFD, and has an essential function in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. VEGFR2 activation promotes the proliferation, survival, migration, and differentiation of endothelial cells. It is activated by binding VEGF, which induces dimerization and autophosphorylation at the following phosphosites, which all contribute to increased phosphotransferase activity. In addition, autophosphorylation of Y801 induces interaction with PIK3R1, autophosphorylation of Y951 and Y1008 induces interaction with PLCg1, autophosphorylation of Y1054, Y996 and Y1059 induces interaction with PLCg1, and autophosphorylation of Y1175 induces interaction with PLCg1, Shb, Shc1 and Shc2. KDR mediates the activation of the ERK1/2 MAP kinase intracellular signalling pathways. VEGFR2 appears to be an oncoprotein (OP). Mutations in the VEGFR2 gene have been observed in patients with hemangioma. Significantly higher VEGFR2 expression was observed in metastatic as compared to non-metastatic human colon cancer cell lines, which directly correlated with increased neovascularization and tumour cell proliferation. Elevated VEGFR2 expression was also correlated with blood vessel count in human intestinal-type gastric cancers, and in tumour cells in primary and metastatic ovarian carcinomas. VEGF signalling is vital to the early stages of tumour progression in mouse models of squamous skin tumours. In addition, inhibition of VEGFR2 resulted in tumour regression through decreased microvasculature and impaired ability to maintain the stem-like characteristic of the tumour cells.
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