Product: VE-Cadherin Antibody
Catalog: AF6265
Description: Rabbit polyclonal antibody to VE-Cadherin
Application: WB IHC IF/ICC
Reactivity: Human, Mouse
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Dog, Chicken
Mol.Wt.: 120kDa; 88kD(Calculated).
Uniprot: P33151
RRID: AB_2835123

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 100ul $280 In stock
 200ul $350 In stock

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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(83%), Zebrafish(92%), Bovine(92%), Horse(100%), Sheep(88%), Dog(92%), Chicken(92%)
VE-Cadherin Antibody detects endogenous levels of total VE-Cadherin.
Cite Format: Affinity Biosciences Cat# AF6265, RRID:AB_2835123.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


7B 4; 7B4; 7B4 antigen; CADH5_HUMAN; Cadherin 5; Cadherin 5 type 2; Cadherin 5, type 2 (vascular endothelium); Cadherin 5, type 2, VE cadherin (vascular epithelium); cadherin, vascular endothelial; cadherin, vascular endothelial, 1; Cadherin-5; Cadherin5; CD 144; CD144; CD144 antigen; CDH 5; CDH5; CDH5 protein; Endothelial specific cadherin; FLJ17376; OTTHUMP00000174777; Vascular endothelial cadherin; Vascular epithelium cadherin; VE Cad; VE-cadherin; VEC;



Endothelial tissues and brain.

This gene is a classical cadherin from the cadherin superfamily and is located in a six-cadherin cluster in a region on the long arm of chromosome 16 that is involved in loss of heterozygosity events in breast and prostate cancer.



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 - P33151 As Substrate

Site PTM Type Enzyme
N61 N-Glycosylation
T62 Phosphorylation
S63 Phosphorylation
Y82 Phosphorylation
N112 N-Glycosylation
N157 N-Glycosylation
T212 Phosphorylation
Y223 Phosphorylation
N362 N-Glycosylation
T392 Phosphorylation
N442 N-Glycosylation
N523 N-Glycosylation
N535 N-Glycosylation
Y658 Phosphorylation P12931 (SRC)
S665 Phosphorylation
S683 Phosphorylation
Y685 Phosphorylation P12931 (SRC)
Y725 Phosphorylation
Y731 Phosphorylation P12931 (SRC)
Y733 Phosphorylation
Y774 Phosphorylation
S776 Phosphorylation
Y784 Phosphorylation

Research Backgrounds


Cadherins are calcium-dependent cell adhesion proteins (By similarity). They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. This cadherin may play a important role in endothelial cell biology through control of the cohesion and organization of the intercellular junctions (By similarity). It associates with alpha-catenin forming a link to the cytoskeleton. Acts in concert with KRIT1 and MPP5 to establish and maintain correct endothelial cell polarity and vascular lumen (By similarity). These effects are mediated by recruitment and activation of the Par polarity complex and RAP1B. Required for activation of PRKCZ and for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction.


Phosphorylated on tyrosine residues by KDR/VEGFR-2. Dephosphorylated by PTPRB (By similarity).


Subcellular Location:

Cell junction. Cell membrane>Single-pass type I membrane protein.
Note: Found at cell-cell boundaries and probably at cell-matrix boundaries. KRIT1 and CDH5 reciprocally regulate their localization to endothelial cell-cell junctions.

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

Endothelial tissues and brain.

Subunit Structure:

Interacts (via cadherin 5 domain) with PTPRB (By similarity). Interacts with TRPC4. Interacts with KRIT1. Interacts with PARD3 (By similarity). Interacts with RTN4 (isoform B). Interacts with MPP5; the interaction promotes MPP5 localization to cell junctions and is required for CDH5-mediated vascular lumen formation and endothelial cell.


Three calcium ions are usually bound at the interface of each cadherin domain and rigidify the connections, imparting a strong curvature to the full-length ectodomain.

Research Fields

· Environmental Information Processing > Signaling molecules and interaction > Cell adhesion molecules (CAMs).   (View pathway)

· Organismal Systems > Immune system > Leukocyte transendothelial migration.   (View pathway)


1). Precisely co-delivery of protein and ROS scavenger with platesomes for enhanced endothelial barrier preservation against myocardial ischemia reperfusion injury. Chemical Engineering Journal [IF=15.1]

2). ZRANB2/SNHG20/FOXK1 Axis regulates Vasculogenic mimicry formation in glioma. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (PubMed: 30744670) [IF=11.3]

Application: WB    Species: human    Sample: U87 and U251 cells

Fig. 1| Endogenous expression of ZRANB2 and effect of ZRANB2 on biological behaviors of glioma cells. c Protein levels of MMP1, MMP9 and VE-Cadherin regulated by ZRANB2 in U87 and U251 cells. Representative protein expressions and corresponding IDVs of MMP1, MMP9, VE-Cadherin in U87 and U251 are shown; data are presented as mean ± SD (n = 3, each group). *P < 0.05 vs. ZRANB2(−)-NC group, **P < 0.01 vs. ZRANB2(−)-NC group, #P < 0.05 vs. ZRANB2(+)-NC group,##P < 0.01 vs. ZRANB2(+)-NC group.

3). Oscillating Magnetic Field Regulates Cell Adherence and Endothelialization Based on Magnetic Nanoparticle-Modified Bacterial Cellulose. ACS Applied Materials & Interfaces (PubMed: 33170636) [IF=9.5]

4). Thymidine phosphorylase promotes malignant progression in hepatocellular carcinoma through pentose Warburg effect. Cell Death & Disease (PubMed: 30674871) [IF=9.0]

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. 6| Effects of the transcriptional pattern of Twist1 to thymidine phosphorylase (TP) on hepatocellular carcinoma (HCC) growth,metastasis, and vasculogenic mimicry (VM) formation in the xenograft model. d Analysis of Twist1, TP, VE–Cad, vascular endothelial growth factor receptor1 (VEGFR1), and VEGFR2 expression levels in xenograft tumors. Images were taken at 400 magnification.

5). Foxq1 promotes metastasis of nasopharyngeal carcinoma by inducing vasculogenic mimicry via the EGFR signaling pathway. Cell Death & Disease (PubMed: 33875643) [IF=9.0]

Application: IF/ICC    Species: mouse    Sample: 5–8F cells

Fig. 7| MiR-124 inhibits the EGFR signaling pathway and VM formation, that could be rescued by Foxq1 expression. E Immunofluorescence staining of Foxq1, EGFR, VE-cadherin, MMP2 and MMP9 in 5–8F cells that overexpressed miR-124, control or simultaneously Foxq1 and miR-124, respectively; scale bars represent 50μm. qRT-PCR (F) and western blot (G) were used to monitor the expression of EGFR signaling pathway and VM-related genes in 5–8F cells that overexpressed miR-124, control or simultaneously Foxq1 and miR-124, respectively.Data are presented as mean ± SD of three independent experiments.

Application: WB    Species: mouse    Sample: 5–8F cells

Fig. 6 |Erlotinib and Nimotuzumab could inhibit Foxq1-induced VM formation and NPC growth and metastasis in vivo.F Statistical results of metastatic nodules of each group; p < 0.001. The expression of related genes in xenograft tumors from each group were monitored by qRT-PCR (G) and western blot (H).

6). Hsp90β promotes aggressive vasculogenic mimicry via epithelial-mesenchymal transition in hepatocellular carcinoma. ONCOGENE (PubMed: 30087438) [IF=8.0]

Application: IHC    Species: human    Sample: HCC cells

Fig. 1| Hsp90βassociates with vasculogenic mimicry and poor prog-nosis in HCC. e Representative images of Hsp90β, Hsp90α, VE-cadherin,E-cadherin, Vimentin, MMP2, and MMP9 expression in VM/Hsp90βnegative and positive HCC tissue samples. All images are repre-sentative.

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.

7). RETRACTED ARTICLE: Hsp90β promotes aggressive vasculogenic mimicry via epithelial–mesenchymal transition in hepatocellular carcinoma. Oncogene (PubMed: 30087438) [IF=8.0]

8). Novel Strategy for Isolation of Mice Bone Marrow–Derived Endothelial Cells (BMECs). Stem Cell Research & Therapy (PubMed: 33941266) [IF=7.5]

Application: WB    Species: mouse    Sample: primary bone marrow endothelial cells

Fig. 4 |Characterization of primary bone marrow endothelial cells by RT-QPCR and immunoblottinge .The immunoblotting analysis of primary bone marrow endothelial after 7 days of cultured further substantiates the purity of endothelial cells with protein ladder (M) (N= 3 indicates independent experiments for RT-qPCR and N=2 for immunoblotting with six mice/group(12 femora and 12 tibias). *p<0.05 **p<0.01, and ***p<0.001

Application: IF/ICC    Species: mouse    Sample: primary bone marrow endothelial cells

Fig. 7| a, b Bone marrow endothelial cell proliferation Ki-67 by flow cytometry analysis and hemocytometer.e The merged immunofluorescence staining of both quiescence BMECs and treated endothelial cells with TNF-α. Scale bar = 5μm, ×20 magnification, N= 3 experimental repeats 3 mice per group, *p< 0.05, **p<0.01, and ***p<0.001

Application: WB    Species: Mice    Sample: bMECs

Fig. 4 Characterization of primary bone marrow endothelial cells by RT-QPCR and immunoblotting: a–d the relative mRNA expression of primary bone marrow endothelial cells compared to CD31 microbead-negative selected cells. The bar chart indicated the fold of the gene expression of primary BMECs compared to the CD31 microbead-negative selected cells. The fold change is quantified by the Pitfall method, followed by a Student’s test comparison between the CD31 microbead-negative selected cells and endothelial cells. P value ≤0.05 considered being statistically significant. e The immunoblotting analysis of primary bone marrow endothelial after 7 days of cultured further substantiates the purity of endothelial cells with protein ladder (M) (N= 3 indicates independent experiments for RT-qPCR and N=2 for immunoblotting with six mice/group (12 femora and 12 tibias). *p<0.05 **p<0.01, and ***p<0.001

Application: IF/ICC    Species: Mice    Sample: BMECs

Fig. 5 Identification of primary bone marrow endothelial cells by immunofluorescence staining: a anti-CD31 (PECAM-1), anti-CD144 (VE-cadherin), anti-CD106 (ICAM-1), and anti-VEGFR2—the cell shows the expression of these endothelial cell-specific molecules. b The mean fluorescence intensity for endothelial cells particular marker in the graph was relatively quantified by ImageJ, which shows the order of the endothelial cell-specific markers (PECAM-1> VE-cadherin > ICAM-1 > VEGFR2, N = 3 experimental repeats with three mice/group (6 femora and 6 tibias), scale bar 5μm, ×20 magnification

9). Protective effects of acarbose against vascular endothelial dysfunction through inhibiting Nox4/NLRP3 inflammasome pathway in diabetic rats. FREE RADICAL BIOLOGY AND MEDICINE (PubMed: 31541678) [IF=7.4]

Application: WB    Species: rat    Sample: endothelial cells

Fig.4. | Acarbose inhibited HG-impaired barrier function in RAECs. RAECs were incubated with HG for 24 hours after the pretreatment with acarbose (3µM) or MCC950 (10µM), or NLRP3 siRNA. Western blots showed the effects of acarbose on the protein expression of ZO-1 and VE-Cadherin (A, B).

Application: IF/ICC    Species: rat    Sample: arterial endothelium

Fig.6. |Acarbose inhibited Nox4/NLRP3 inflammasome in the arterial endothelium of diabetic rats .Male SD rats were fed HFD and a low dose of STZ (40mg/kg, i.p.) to develop a rat model of T2DM that were treated with acarbose (30mg/kg/d) and MCC950(3mg/kg/d) for 5 weeks. Representative immunofluorescent images and summarized data showed the role of acarbose and MCC950 on the expression of ZO-1 and VE-Cadherin in the arterial endothelium (A-B).

10). Sema3A and HIF1α co-overexpressed iPSC-MSCs/HA scaffold facilitates the repair of calvarial defect in a mouse model. JOURNAL OF CELLULAR PHYSIOLOGY (PubMed: 32012286) [IF=5.6]

Application: IF/ICC    Species: Mice    Sample: calvariae tissues

FIGURE 6 The expression of RUNX2 and VE‐Cadherin in calvarial defect tissue of mice implanted with HA scaffold combined with LV‐NC or LV‐Sema3A/HIF1α infected iPSC‐MSCs. Immunofluorescence analysis the expression of RUNX2 (a) and VE‐Cadherin (b) in mice defect implanted the LV‐NC‐iPSC‐MSCs/HA scaffold or LV‐Sema3A/HIF1α‐iPSC‐MSCs/HA scaffold at 8 weeks after surgery (scale bar = 100 μm). HA, hydroxyapatite; HIF1α, hypoxia‐inducible factor‐1α; iPSC, induced pluripotent stem cell; LV, lentivirus; MSC, mesenchymal stem or stromal cell; RUNX2, runt‐related transcription factor 2; Sema3A, semaphorin 3A

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