Product: VEGFR2 Antibody
Catalog: AF6281
Source: Rabbit
Application: WB, IHC, IF/ICC
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Bovine, Sheep, Rabbit, Dog
Mol.Wt.: 180kDa; 152kD(Calculated).
Uniprot: P35968
RRID: AB_2835132

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:200
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Pig(82%), Bovine(82%), Sheep(82%), Rabbit(82%), Dog(82%)
VEGFR2 Antibody detects endogenous levels of total VEGFR2.
Cite Format: Affinity Biosciences Cat# AF6281, RRID:AB_2835132.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
PBS, pH 7.4,50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


CD309; CD309 antigen; EC; Fetal liver kinase 1; FLK-1; FLK1; FLK1, mouse, homolog of; Kdr; Kinase insert domain receptor (a type III receptor tyrosine kinase); Kinase insert domain receptor; KRD1; Ly73; Protein tyrosine kinase receptor FLK1; Protein-tyrosine kinase receptor flk-1; soluble VEGFR2; Tyrosine kinase growth factor receptor; Vascular endothelial growth factor receptor 2; VEGFR 2; VEGFR; VEGFR-2; VEGFR2; VGFR2_HUMAN;



Detected in cornea (at protein level). Widely expressed.

VEGFR-2 is a receptor tyrosine kinase of the VEGFR family. High affinity receptor for VEGF and VEGF-C. Ligand binding induces autophosphorylation and activation. Activated receptor recruits proteins including Shc, GRB2, PI3K, Nck, SHP-1 and SHP-2.



Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P35968 As Substrate

Site PTM Type Enzyme
N143 N-Glycosylation
S229 Phosphorylation Q00535 (CDK5)
N245 N-Glycosylation
N318 N-Glycosylation
S711 Phosphorylation
Y801 Phosphorylation
Y822 Phosphorylation
S825 Phosphorylation
Y951 Phosphorylation P35968 (KDR)
K960 Acetylation
S982 Phosphorylation
S984 Phosphorylation
Y996 Phosphorylation P35968 (KDR)
Y1054 Phosphorylation P35968 (KDR)
K1055 Ubiquitination
Y1059 Phosphorylation P35968 (KDR)
Y1175 Phosphorylation P12931 (SRC) , P35968 (KDR)
Y1214 Phosphorylation P35968 (KDR)
T1217 Phosphorylation
Y1223 Phosphorylation
S1235 Phosphorylation
T1238 Phosphorylation
S1279 Phosphorylation
S1281 Phosphorylation
S1288 Phosphorylation
S1290 Phosphorylation
Y1305 Phosphorylation P35968 (KDR)
Y1309 Phosphorylation P35968 (KDR)
Y1319 Phosphorylation P35968 (KDR)

PTMs - P35968 As Enzyme

Substrate Site Source
P07737 (PFN1) Y129 Uniprot
P35916 (FLT4) Y1230 Uniprot
P35916 (FLT4) Y1231 Uniprot
P35916 (FLT4) Y1265 Uniprot
P35916 (FLT4) Y1333 Uniprot
P35968 (KDR) Y951 Uniprot
P35968 (KDR) Y996 Uniprot
P35968 (KDR) Y1054 Uniprot
P35968 (KDR) Y1059 Uniprot
P35968 (KDR) Y1175 Uniprot
P35968 (KDR) Y1214 Uniprot
P35968 (KDR) Y1305 Uniprot
P35968 (KDR) Y1309 Uniprot
P35968 (KDR) Y1319 Uniprot

Research Backgrounds


Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFC and VEGFD. Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. Promotes proliferation, survival, migration and differentiation of endothelial cells. Promotes reorganization of the actin cytoskeleton. Isoforms lacking a transmembrane domain, such as isoform 2 and isoform 3, may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Isoform 2 plays an important role as negative regulator of VEGFA- and VEGFC-mediated lymphangiogenesis by limiting the amount of free VEGFA and/or VEGFC and preventing their binding to FLT4. Modulates FLT1 and FLT4 signaling by forming heterodimers. Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, reorganization of the actin cytoskeleton and activation of PTK2/FAK1. Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. Phosphorylates PLCG1. Promotes phosphorylation of FYN, NCK1, NOS3, PIK3R1, PTK2/FAK1 and SRC.



Ubiquitinated. Tyrosine phosphorylation of the receptor promotes its poly-ubiquitination, leading to its degradation via the proteasome or lysosomal proteases.

Autophosphorylated on tyrosine residues upon ligand binding. Autophosphorylation occurs in trans, i.e. one subunit of the dimeric receptor phosphorylates tyrosine residues on the other subunit. Phosphorylation at Tyr-951 is important for interaction with SH2D2A/TSAD and VEGFA-mediated reorganization of the actin cytoskeleton. Phosphorylation at Tyr-1175 is important for interaction with PLCG1 and SHB. Phosphorylation at Tyr-1214 is important for interaction with NCK1 and FYN. Dephosphorylated by PTPRB. Dephosphorylated by PTPRJ at Tyr-951, Tyr-996, Tyr-1054, Tyr-1059, Tyr-1175 and Tyr-1214.

The inhibitory disulfide bond between Cys-1024 and Cys-1045 may serve as a specific molecular switch for H(2)S-induced modification that regulates KDR/VEGFR2 function.

Subcellular Location:

Cell junction. Endoplasmic reticulum.
Note: Localized with RAP1A at cell-cell junctions (By similarity). Colocalizes with ERN1 and XBP1 in the endoplasmic reticulum in endothelial cells in a vascular endothelial growth factor (VEGF)-dependent manner (PubMed:23529610).

Cell membrane>Single-pass type I membrane protein. Cytoplasm. Nucleus. Cytoplasmic vesicle. Early endosome.
Note: Detected on caveolae-enriched lipid rafts at the cell surface. Is recycled from the plasma membrane to endosomes and back again. Phosphorylation triggered by VEGFA binding promotes internalization and subsequent degradation. VEGFA binding triggers internalization and translocation to the nucleus.



Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Detected in cornea (at protein level). Widely expressed.

Subunit Structure:

Homodimer in the presence of bound dimeric VEGFA, VEGFC or VEGFD ligands; monomeric in the absence of bound ligands. Can also form heterodimers with FLT1/VEGFR1 and KDR/VEGFR2. Interacts (tyrosine phosphorylated) with LFYN, NCK1, PLCG1. Interacts (tyrosine-phosphorylated active form preferentially) with DAB2IP (via C2 domain and active form preferentially); the interaction occurs at the late phase of VEGFA response and inhibits KDR/VEGFR2 activity. Interacts with SHBSH2D2A/TSAD, GRB2, MYOF, CBL and PDCD6. Interacts (via C-terminus domain) with ERN1 (via kinase domain); the interaction is facilitated in a XBP1 isoform 1- and vascular endothelial growth factor (VEGF)-dependent manner in endothelial cells. Interacts (via juxtamembrane region) with chaperone PDCL3 (via thioredoxin fold region); the interaction leads to increased KDR/VEGFR2 abundance through inhibition of its ubiquitination and degradation. Interacts (tyrosine phosphorylated) with CCDC88A/GIV (via SH2-like region); binding requires autophosphorylation of the KDR/VEGFR2 C-terminal region.

(Microbial infection) Interacts with HIV-1 Tat.


The second and third Ig-like C2-type (immunoglobulin-like) domains are sufficient for VEGFC binding.

Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily.

Research Fields

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.


1). Xia J et al. Mitochondrial Protein UCP1 Inhibits the Malignant Behaviors of Triple-negative Breast Cancer through Activation of Mitophagy and Pyroptosis. Int J Biol Sci 2022 Apr 18;18(7):2949-2961. (PubMed: 35541900) [IF=10.750]

2). Zhang Q et al. Thymidine phosphorylase promotes malignant progression in hepatocellular carcinoma through pentose Warburg effect. Cell Death Dis 2019 Jan 17;10(2):43 (PubMed: 30674871) [IF=9.685]

Application: WB    Species: human    Sample: PLC-PRF-5 cells

Fig. 3| Enzymatic metabolism of extracellular dT regulated by thymidine phosphorylase (TP)affects tumor functions related to vasculogenic mimicry (VM) formation in hepatocellular carcinoma cells..e Western blot analysis of the expression levels of VE–Cad, vascular endothelial growth factor receptor 1 (VEGFR1), and VEGFR2 influenced by overexpressing TP and adding dT in glucose-free cultured PLC-PRF-5 cells. The ratio of densitometry value to the corresponding glyceraldehyde 3-phosphate dehydrogenase (GAPDH) value was used to indicate the relative protein expression. NG means “No Glucose” (mean ± SD; n = 3 in triplicate; **P < 0.01)

Application: IHC    Species: human    Sample: HCC

Fig. 5 |Twist1 relies on thymidine phosphorylase (TP) to promote hepatocellular carcinoma (HCC) malignant progression. HCC samples were divided into four groups of Twist1/TP (−/−), Twist1/TP (−/+), Twist1/TP (+/−), and Twist1/TP (+/+) according to the Twist1/TP expression levels. D Analysis of the HCC specimens by IHC. VE–Cad, vascular endothelial growth factor receptor 1 (VEGFR1), and VEGFR2 were minimally expressed in the Twist1- and TP-negative expression groups. When Twist1 and TP were individually or both positively expressed, the expression levels of the three marker proteins increased.

3). Meng J et al. Hsp90β promotes aggressive vasculogenic mimicry via epithelial-mesenchymal transition in hepatocellular carcinoma. Oncogene 2018 Aug 7 (PubMed: 30087438) [IF=8.756]

Application: WB    Species: human    Sample: PLC-PRF-5 cells

Fig. 5| Hsp90β promotes Twist1 nuclear translocation and binding to VE-cadherin promoter to increase VM-related gene networks. eWestern blot analysis of VM and EMT-related markers, including VE-cadherin, VEGFR1, VEGFR2, E-cadherin, Vimentin, MMP2, and MMP9 in PLC-PRF-5 cells overexpressed Hsp90β or under lack of Twist1.

4). Chen L et al. Electroacupuncture Reduces Oocyte Number and Maintains Vascular Barrier Against Ovarian Hyperstimulation Syndrome by Regulating CD200. Front Cell Dev Biol 2021 Feb 22;9:648578. (PubMed: 33693006) [IF=6.081]

Application: WB    Species: human    Sample: HUVECs

FIGURE 6 | Effects of CD200Fc on inflammatory response pathway in KGN cells and vascular permeability-related protein and cell cytoskeleton in HUVECs.. (C) The levels of vasoactive proteins VEGF and VEGFR2, and cell junction proteins Occludin, Claudin 5,and ZO-1 were examined by western blotting.

5). Qian K et al. β-Sitosterol Inhibits Rheumatoid Synovial Angiogenesis Through Suppressing VEGF Signaling Pathway. Front Pharmacol 2022 Feb 28;12:816477. (PubMed: 35295740) [IF=5.810]

Application: WB    Species: Human    Sample: HUVECs

FIGURE 4 The effect of VEGF signaling pathway in TNF-α-induced HUVECs regulated by BSS. (A) GSEA analysis of KEGG signaling pathway in the GSE121894 dataset. The structural interactions between VEGFR2 and BSS (B) and between VEGFR2 and axitinib (C) were described by molecular simulation, and binding affinity of VEGFR2 with BSS and axitinib is shown in Table 1. (D) p-VEGFR2 and VEGFR2 protein levels in HUVECs (on TNF-α 20 ng/ml for 1 h) intervened with BSS dosage groups were detected by immunoblotting and the relative expression levels (E) of proteins were corrected by GAPDH (n = 3). (F) p-VEGFR2 and VEGFR2 protein levels in HUVECs intervened with BSS and axitinib were detected by immunoblotting, and the relative expression levels (G) of proteins were corrected by GAPDH (n = 3). All data are shown as the mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, n.s. = not significant.

Application: IHC    Species: Mice    Sample: synovial tissues

FIGURE 6 Effect of BSS on immunohistochemistry of CD31, VEGFR2, and P-VEGFR2 on experimental arthritis. (A) CD31 immunohistochemical staining of the ankle joints in each group, and the optical density value (B) analysis using ImageJ (n = 6) (×200, scale bar = 50 μm). (C) VEGFR2 immunohistochemical staining of the ankle joints in each group, and the optical density value (D) analysis using ImageJ (n = 6) (×200, scale bar = 50 μm). (E) p-VEGFR2 immunohistochemical staining of the ankle joints in each group, and (F) the optical density value analysis using ImageJ (n = 6) (×200, scale bar = 50 μm). All data are shown as the mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, n.s. = not significant.

6). Ling L et al. Important role of the SDF-1/CXCR4 axis in the homing of systemically transplanted human amnion-derived mesenchymal stem cells (hAD-MSCs) to ovaries in rats with chemotherapy-induced premature ovarian insufficiency (POI). Stem Cell Res Ther 2022 Feb 23;13(1):79. (PubMed: 35197118) [IF=5.116]

Application: IHC    Species: Human    Sample: ovarian tissue

Fig. 7 Effects of hAD-MSCs on ovarian injuries induced by chemotherapy in POI rats after blocking the SDF-1/CXCR4 axis. a Changes in the ovarian tissue were analysed using HE staining (×100 and ×200). b The number of follicles at different stages was counted and compared in the control, POI, hAD-MSCs and hAD-MSCs + AMD3100 groups (n = 10). c Ovarian granulosa cell (GC) apoptosis was tested using the TUNEL assay (×100 and ×400). d The expression levels of Bax, Bcl-2, cleaved-caspase-3, VEGF and VEGFR2 in the ovaries were detected using immunohistochemical staining (×100 and ×400). e–i Semiquantitative analyses of Bax, Bcl-2, cleaved-caspase-3, VEGF and VEGFR2 levels in the ovaries from each group are shown (n = 10). Each dot in the graphs (e–i) represents the value obtained from ten high-power fields (HPFs) randomly chosen from five sections in each group. The bars and error bars in graphs (e–i) indicate the medians and ranges, respectively. Brown cells represent immunostained cells. Representative images are shown. *P < 0.05 and **P < 0.01. Scale bars = 100 μm

7). Deng S et al. The regulatory roles of VEGF-Notch signaling pathway on aplastic anemia with kidney deficiency and blood stasis. J Cell Biochem 2018 Sep 19 (PubMed: 30230583) [IF=4.480]

8). Gu M. et al. IL13Rα2 siRNA inhibited cell proliferation, induced cell apoptosis, and suppressed cell invasion in papillary thyroid carcinoma cells. Onco Targets Ther 2018 Mar 9;11:1345-1352 (PubMed: 29563812) [IF=4.345]

9). Wu CZ et al. HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma. Onco Targets Ther 2018 Aug 1;11:4501-4510 (PubMed: 30122942) [IF=4.345]

Application: WB    Species: human    Sample: HUVEC

Figure 5 |The effects of HMGB1 on RCC-stimulated VEGF and VEGFR2 expressions in HUVEC.(C, D) The effects of HMGB1/sRAGE on RCC-stimulated VEGF and VEGFR2 proteins expression in HUVEC were detected by Western blot analysis. *P,0.05, **P,0.01 vs Con-siRNA group; ##P,0.01 vs Con-Vec group; ^^P,0.01 vs sRAGE group.

10). Huang X et al. SU5416 attenuated lipopolysaccharide-induced acute lung injury in mice by modulating properties of vascular endothelial cells. Drug Des Devel Ther 2019 May 23;13:1763-1772 (PubMed: 31213766) [IF=4.319]

Application: WB    Species: mouse    Sample: lung

Figure 3 |TLR4/NF-κB signaling was involved in the progression of LPS-stimulated ALI. (A) Immunohistochemical staining of CD31 in LPS-stimulated WT and TLR4−/- mice after treatment with DXM and/or SU5416+DXM.. (B) Mice were treated with DXM and/or SU5416 for 12 hours, and the expressions of TLR4, p-p65, NF-κB, p-VEGFR2,VEGF2R, p53, Bcl-2, and β-actin in lung tissues were detected with Western blot

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