Product Name: KDR (135-150)
Product Number: PE-01AVM95
Size: 200 µg      Price:51.00
1 mg      $US102.00
5 mg      224.00
Peptide Name: KDR (135-150)

Product Use: Services as a blocking peptide for use with the VGFR2-1 rabbit polyclonal antibody (Cat. No.: AB-NK245-1) that is also available from Kinexus. The peptide sequence is located in the extracellular domain of the receptor.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: VVYITENKNKTVVIPC

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1819.1 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: KDR pan-specific antibody (Cat. No.: AB-NK245-1)

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.