Phospho-VEGF Receptor 2 (Tyr951) Antibody [F15G14]

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
230 kDa

Positive Control	Recombinant human GST-VEGF Receptor 2 (Val789-Val1356)
Negative Control

Datasheet & SDS

Biological Description

Specificity
Phospho-VEGF Receptor 2 (Tyr951) Antibody [F15G14] detects endogenous levels of total VEGF receptor 2 protein only when it is phosphorylated at Tyr951.

Clone
F15G14

Synonym(s)
Vascular endothelial growth factor receptor 2; VEGFR-2; Fetal liver kinase 1 (FLK-1); Kinase insert domain receptor (KDR); Protein-tyrosine kinase receptor flk-1; CD309; KDR; FLK1; VEGFR2

Background
Phospho-VEGF Receptor 2 (Tyr951) represents a critical signaling node in the regulation of endothelial cell function and angiogenesis. VEGFR2, also known as KDR or Flk-1, is a receptor tyrosine kinase of the PDGFR family that mediates the effects of VEGF-A in vascular development and remodeling. Upon VEGF-A binding, VEGFR2 undergoes dimerization and autophosphorylation at multiple tyrosine residues, including Tyr951, which is located within the kinase insert domain adjacent to the activation loop. Phosphorylation at Tyr951 creates a docking site for the T-cell-specific adaptor protein (TSAd/VRAP/LAD), initiating the assembly of a VEGFR2-pY951-TSAd-Src signaling complex. This complex activates c-Src via phosphorylation at Tyr418 and dephosphorylation at Tyr527, thereby stimulating downstream PI3K-Akt pathways. The result is enhanced endothelial cell survival, increased vascular permeability, directed migration, and actin cytoskeletal reorganization necessary for cell motility. In tumors, TSAd and pY951 signaling are upregulated, thereby supporting abnormal vessel growth. Disruption of this pathway, through Y951F mutation, pY951-mimicking peptides, or TSAd silencing, impedes VEGF-A-induced endothelial migration, decreases tumor vascularization, and suppresses tumor growth in TSAd-deficient models.

Background

Phospho-VEGF Receptor 2 (Tyr951) represents a critical signaling node in the regulation of endothelial cell function and angiogenesis. VEGFR2, also known as KDR or Flk-1, is a receptor tyrosine kinase of the PDGFR family that mediates the effects of VEGF-A in vascular development and remodeling. Upon VEGF-A binding, VEGFR2 undergoes dimerization and autophosphorylation at multiple tyrosine residues, including Tyr951, which is located within the kinase insert domain adjacent to the activation loop. Phosphorylation at Tyr951 creates a docking site for the T-cell-specific adaptor protein (TSAd/VRAP/LAD), initiating the assembly of a VEGFR2-pY951-TSAd-Src signaling complex. This complex activates c-Src via phosphorylation at Tyr418 and dephosphorylation at Tyr527, thereby stimulating downstream PI3K-Akt pathways. The result is enhanced endothelial cell survival, increased vascular permeability, directed migration, and actin cytoskeletal reorganization necessary for cell motility. In tumors, TSAd and pY951 signaling are upregulated, thereby supporting abnormal vessel growth. Disruption of this pathway, through Y951F mutation, pY951-mimicking peptides, or TSAd silencing, impedes VEGF-A-induced endothelial migration, decreases tumor vascularization, and suppresses tumor growth in TSAd-deficient models.

References
https://pubmed.ncbi.nlm.nih.gov/15962004/ https://pubmed.ncbi.nlm.nih.gov/33304904/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%