Product: VEGFA Antibody
Catalog: AF5131
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 16-20kD,25-30kD,40-45kD; 27kD(Calculated).
Uniprot: P15692
RRID: AB_2837617

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
*Tips:

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.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(89%), Horse(89%), Sheep(90%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
VEGFA Antibody detects endogenous levels of total VEGFA.
RRID:
AB_2837617
Cite Format: Affinity Biosciences Cat# AF5131, RRID:AB_2837617.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

Folliculostellate cell-derived growth factor; Glioma-derived endothelial cell mitogen; MGC70609; MVCD1; Vascular endothelial growth factor A; vascular endothelial growth factor A121; vascular endothelial growth factor A165; vascular endothelial growth factor; Vascular permeability factor; VEGF A; Vegf; VEGF-A; VEGF120; Vegfa; VEGFA_HUMAN; VPF;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P15692 VEGFA_HUMAN:

Isoform VEGF189, isoform VEGF165 and isoform VEGF121 are widely expressed. Isoform VEGF206 and isoform VEGF145 are not widely expressed. A higher level expression seen in pituitary tumors as compared to the pituitary gland.

Description:
Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth. Induces endothelial cell proliferation, promotes cell migration, inhibits apoptosis and induces permeabilization of blood vessels. Binds to the FLT1/VEGFR1 and KDR/VEGFR2 receptors, heparan sulfate and heparin
Sequence:
MNFLLSWVHWSLALLLYLHHAKWSQAAPMAEGGGQNHHEVVKFMDVYQRSYCHPIETLVDIFQEYPDEIEYIFKPSCVPLMRCGGCCNDEGLECVPTEESNITMQIMRIKPHQGQHIGEMSFLQHNKCECRPKKDRARQEKKSVRGKGKGQKRKRKKSRYKSWSVYVGARCCLMPWSLPGPHPCGPCSERRKHLFVQDPQTCKCSCKNTDSRCKARQLELNERTCRCDKPRR

Predictions

Predictions:

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.

Species
Results
Score
Pig
100
Dog
100
Rabbit
100
Sheep
90
Horse
89
Bovine
89
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P15692 As Substrate

Site PTM Type Enzyme

Research Backgrounds

Function:

Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth. Induces endothelial cell proliferation, promotes cell migration, inhibits apoptosis and induces permeabilization of blood vessels. Binds to the FLT1/VEGFR1 and KDR/VEGFR2 receptors, heparan sulfate and heparin. NRP1/Neuropilin-1 binds isoforms VEGF-165 and VEGF-145. Isoform VEGF165B binds to KDR but does not activate downstream signaling pathways, does not activate angiogenesis and inhibits tumor growth. Binding to NRP1 receptor initiates a signaling pathway needed for motor neuron axon guidance and cell body migration, including for the caudal migration of facial motor neurons from rhombomere 4 to rhombomere 6 during embryonic development (By similarity).

Subcellular Location:

Secreted.
Note: VEGF121 is acidic and freely secreted. VEGF165 is more basic, has heparin-binding properties and, although a significant proportion remains cell-associated, most is freely secreted. VEGF189 is very basic, it is cell-associated after secretion and is bound avidly by heparin and the extracellular matrix, although it may be released as a soluble form by heparin, heparinase or plasmin.

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

Isoform VEGF189, isoform VEGF165 and isoform VEGF121 are widely expressed. Isoform VEGF206 and isoform VEGF145 are not widely expressed. A higher level expression seen in pituitary tumors as compared to the pituitary gland.

Subunit Structure:

Homodimer; disulfide-linked. Also found as heterodimer with PGF (By similarity). Interacts with NRP1.

Family&Domains:

Belongs to the PDGF/VEGF growth factor family.

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 > HIF-1 signaling pathway.   (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 > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

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

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

· Human Diseases > Cancers: Specific types > Renal cell carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). Li X et al. Upregulation of BCL-2 by acridone derivative through gene promoter i-motif for alleviating liver damage of NAFLD/NASH. Nucleic Acids Res 2020 Jul 25;gkaa615. (PubMed: 32710621) [IF=19.160]

Application: WB    Species: human    Sample: HepG2

Figure 3. Effect of A22 on gene transcription and translation in HepG2 cells. The mRNA levels of BCL-2 and BAX (A), as well as C-KIT, KRAS, C-MYC and VEGF (B) in HepG2 cells were analyzed by using qRT-PCR after incubation with increasing concentration of A22 for 12 h. (C) Effects of A22 on protein expressions of C-MYC, VEGF, C-KIT and BCL-2 in the presence or absence of increasing concentration of A22 for 24 h, which were quantitatively analyzed

2). Chen X et al. SMURF1-mediated ubiquitination of ARHGAP26 promotes ovarian cancer cell invasion and migration. Exp Mol Med 2019 Apr 19;51(4):46 (PubMed: 31004081) [IF=12.153]

Application: WB    Species: human    Sample: A2780 and HEY cells

Fig. 3 | ARHGAP26 upregulation inhibited the ovarian cancer cell invasion and migration. A2780 and HEY cells were transduced with recombined ARHGAP26 expression lentivirus or control lentivirus (blank vector). Cell migration and invasion of A2780 (a, b) and HEY cells (c, d) were detected via Transwell analysis, and the expression of GTP-RhoA, total RhoA, β-catenin, VEGF, MMP2, and MMP7 in A2780 and HEY cells was detected via western blotting (e–g).

3). Ai XY et al. Phenytoin silver: a new nanocompound for promoting dermal wound healing via comprehensive pharmacological action. Theranostics 2017 Jan 5;7(2):425-435 (PubMed: 28255340) [IF=11.600]

Application: WB    Species: human    Sample:

Figure 6. PnAg regulates gp130/Jak/Stat3 signaling pathway (A) and (B) NIH-3T3 and HaCat Cells were treated with PnAg at different concentrations and cell viability was tested using MTT analysis. (C) Wound healing assay reflected the effect of PnAg on cell migration. (D) Binding mode of PnAg in the active pocket of gp130. (E) and (F) MMPs activity and expression levels of Stat3, VEGF, TGFB-1, and TGFB1 detected using zymographic and Western blot assays. (G) Diagram of the proposed function of PnAg in wound inflammation and re-epithelialization controls.

4). Yang W et al. Co‐overexpression of VEGF and GDNF in adipose‐derived stem cells optimizes therapeutic effect in neurogenic erectile dysfunction model. Cell Prolif 2020 Feb;53(2):e12756. (PubMed: 31943490) [IF=8.755]

Application: WB    Species: rats    Sample: Adipose-derived stem cells (ADSCs)

FIGURE 1  Genetically modified ADSCs produced more VEGF and GDNF. A,B, Morphology of ADSCs in passage 0 and passage 3. C,D, Adipose-derived stem cells exhibited pluripotency after induction, as evidenced by the presence of typical phenotype of osteocytes (stained with Alizarin Red S) and the typical phenotype of adipocytes (stained with Oil Red O). E, Flow cytometry showed the ADSCs expressed more stem cell markers (CD90, CD44a and CD29), but less haematopoietic and endothelial markers (CD34, CD11b and CD45). F, Immunofluorescence analysis of the expression of RFP in transfected ADSCs. G,H, Western blot analysis showed markedly increased the levels of VEGF in transfected ADSCs. I, Immunofluorescence analysis of the expression of GFP in transfected ADSCs. J,K, Western blot analysis showed increased the levels of GDNF in transfected ADSCs. L, Immunofluorescence of ADSCs that co-expressed RFP and GFP. M,N, Western blot analysis of ADSCs co-transfected with VEGF and GDNF. All values are represented as the mean ± SD from three independent experiments, each with three replicates. Statistically significant differences from the control group are denoted as follows: ***P < .001, **P < .01 and *P < .05 (independent samples t test)

Application: WB    Species: Rat    Sample: epididymal adipose tissue

Figure 1 Genetically modified ADSCs produced more VEGF and GDNF. A,B, Morphology of ADSCs in passage 0 and passage 3. C,D, Adipose‐derived stem cells exhibited pluripotency after induction, as evidenced by the presence of typical phenotype of osteocytes (stained with Alizarin Red S) and the typical phenotype of adipocytes (stained with Oil Red O). E, Flow cytometry showed the ADSCs expressed more stem cell markers (CD90, CD44a and CD29), but less haematopoietic and endothelial markers (CD34, CD11b and CD45). F, Immunofluorescence analysis of the expression of RFP in transfected ADSCs. G,H, Western blot analysis showed markedly increased the levels of VEGF in transfected ADSCs. I, Immunofluorescence analysis of the expression of GFP in transfected ADSCs. J,K, Western blot analysis showed increased the levels of GDNF in transfected ADSCs. L, Immunofluorescence of ADSCs that co‐expressed RFP and GFP. M,N, Western blot analysis of ADSCs co‐transfected with VEGF and GDNF. All values are represented as the mean ± SD from three independent experiments, each with three replicates. Statistically significant differences from the control group are denoted as follows: ***P < .001, **P < .01 and *P < .05 (independent samples t test)

Application: IHC    Species: Rat    Sample: MPG and pen

Figure 3 The expression of VEGF and GDNF in the MPG and penis after transplantation of GM‐ADSCs. A, Immunohistochemical staining of rat MPG tissue cross‐sections from each animal in the respective groups using specific VEGF and GDNF antibodies. Arrows indicate typical immune‐positive cells. B,C, Immunohistochemical score was obtained by analysing the staining intensity and positive rate of VEGF and GDNF. D, After 14 d, transfected ADSCs were visible in the MPG and corpus cavernosa. E, Representative immunofluorescence staining of GDNF (green) in a penile mid‐shaft specimen 2 wk after BCNI and treatment. F, Quantitative analysis of the GDNF‐positive area. G,H, Representative immunofluorescence of VEGF in a penile mid‐shaft specimen, and quantitative analysis of the VEGF immunofluorescence‐positive area. Data are depicted as the mean ± SD from n = 6 animals per group (*P < .05). Immunofluorescence was analysed using one‐way ANOVA followed by the S‐N‐K test. Quantitative analysis of immunohistochemistry was performed using the Kruskal‐Wallis H test

Application: IF/ICC    Species: Rat    Sample: MPG and pen

Figure 3 The expression of VEGF and GDNF in the MPG and penis after transplantation of GM‐ADSCs. A, Immunohistochemical staining of rat MPG tissue cross‐sections from each animal in the respective groups using specific VEGF and GDNF antibodies. Arrows indicate typical immune‐positive cells. B,C, Immunohistochemical score was obtained by analysing the staining intensity and positive rate of VEGF and GDNF. D, After 14 d, transfected ADSCs were visible in the MPG and corpus cavernosa. E, Representative immunofluorescence staining of GDNF (green) in a penile mid‐shaft specimen 2 wk after BCNI and treatment. F, Quantitative analysis of the GDNF‐positive area. G,H, Representative immunofluorescence of VEGF in a penile mid‐shaft specimen, and quantitative analysis of the VEGF immunofluorescence‐positive area. Data are depicted as the mean ± SD from n = 6 animals per group (*P < .05). Immunofluorescence was analysed using one‐way ANOVA followed by the S‐N‐K test. Quantitative analysis of immunohistochemistry was performed using the Kruskal‐Wallis H test

5). Yang W et al. Co‐overexpression of VEGF and GDNF in adipose‐derived stem cells optimizes therapeutic effect in neurogenic erectile dysfunction model. Cell Prolif 2020 Feb;53(2):e12756. (PubMed: 31943490) [IF=8.755]

6). He WH et al. Estradiol promotes trophoblast viability and invasion by activating SGK1. Biomed Pharmacother 2019 Sep;117:109092 (PubMed: 31203134) [IF=7.419]

7). Fan X et al. Design, synthesis and biological evaluation of N-anthraniloyl tryptamine derivatives as pleiotropic molecules for the therapy of malignant glioma. Eur J Med Chem 2021 Oct 15;222:113564. (PubMed: 34091208) [IF=7.088]

Application: WB    Species: Rat    Sample: Tumor tissue

Fig. 10. NP16 suppressed the growth of tumor in a rat C6 glioma orthotopic model in vivo. All data are expressed as the mean ± SD of individual groups of rats (n ¼ 5 per group). (A) Images of MRI of all tumors on day 12 after tumor cell implantation. (B) Image of dissected tumors from the brains on day 13 after tumor cell implantation. (C) Body weight variation curve for every rat was recorded every three days after modelling. #P < 0.05, ##P < 0.01, ###P < 0.001 vs Sham; *P < 0.05, **P < 0.01, ***P < 0.001 vs C6 group. (D) The weights of dissected tumors on day 13 after tumor cell implantation. *P < 0.05 vs C6 group. (E) The volumes of peeled tumors on day 13 after tumor cell implantation. Tumor volume was calculated by length  width [2]  0.50 using radial measurements performed with calipers. *P < 0.05, **P < 0.01 vs C6 group. (F) Tumor tissue lysates were analyzed by Western blot. (G) The quantification of protein expressions of E-cadherin, VEGF-A and p-STAT3 in tumor lysates by Image J. ##P < 0.01 vs Sham; **P < 0.01, ***P < 0.001 vs C6 group. (H) Effect of NP16 on PGE2 level in peeled tumors measured by ELISA. ##P < 0.01 vs Sham; *P < 0.05 vs C6 group.

8). Li J et al. N-2-(phenylamino) benzamide derivatives as novel anti-glioblastoma agents: Synthesis and biological evaluation. Eur J Med Chem 2021 Sep 10;226:113817. (PubMed: 34537445) [IF=7.088]

Application: WB    Species: Rat    Sample: tumor tissue

Fig. 10. I-1 and I-8 decreased PGE2 production, VEGFA expression, STAT3 activation in a rat C6 glioma orthotopic model in vivo. A. I-1 reduced p-STAT3 expression of tumor regions. Magnification: 47.3 , Scale ¼ 50 mm. The blue fluorescence represents the nucleus and the red fluorescence represents the expression of p-STAT3. B. I-1 and I-8 decreased PGE2 production measured by ELISA method. C. The ratio of p-STAT3/STAT3 from Western blot assay. D. Statistical data of VEGFA expression from Western blot assay. E. Western blot images of p-STAT3, STAT3, VEGFA, b-actin. Data are presented as the mean ± SD of at least three independent assays. *P < 0.05; **P < 0.01, ***P < 0.001 compared with the C6 group. ###P < 0.001 compared with the sham group. TMZ represents temozolomide.

9). Jiang L et al. The effect of MMP-2 inhibitor 1 on osteogenesis and angiogenesis during bone regeneration. Front Cell Dev Biol 2021 Jan 22;8:596783. (PubMed: 33553142) [IF=6.081]

Application: WB    Species: human    Sample: HUVECs

FIGURE 4 | The effects of MMP2-I1 on levels of angio-specific genes and proteins of HUVECs. (A) The expression of VEGF mRNA was determined by qPCR at days 1 and 3. (B) The expression of CD31 mRNA. (C) The expression of EMCN mRNA. (D–G) The expression of VEGF, EMCN and CD31 proteins were determined by Western blot analysis for 3 and 7 days. All the data were confirmed by three repeated tests. Data were mean ± S.D. *p < 0.05 vs. the control group at the same day.#p < 0.05 vs. the control group at the same day

10). Sun X et al. Changes in neurological and pathological outcomes in a modified rat spinal cord injury model with closed canal. Neural Regen Res 2020 Apr;15(4):697-704 (PubMed: 31638094) [IF=6.058]

Application: IHC    Species: Rat    Sample: immunoreactive cells

Figure 5 Influence of spinal canal environment on changes in immunohistochemical staining after primary spinal cord injury in different groups at 7 days post-operation. (A) Immunohistochemical staining: The immunoreactive cells were stained yellow and observed in the spinal cord. Typical immunoreactive cells are marked by arrows. Few immunoreactive cells were seen in the sham group, and the number of immunoreactive cells was higher in the SCIC group than in the SCIO group. Scale bars: 500 μm. (B) Percentage of immunoreactive cells in the injured spinal cord: The percentages of HIF-1α- and VEGF-immunoreactive cells were higher in the SCIC group than in the SCIO group (*P < 0.05; mean ± SD, n = 8; one-way analysis of variance followed by the Bonferroni correction in various groups). HIF-1α: Hypoxia-inducible factor 1α; SCIC: spinal cord injury with closed canal; SCIO: spinal cord injury with open canal; VEGF: vascular endothelial growth factor.

Application: WB    Species: Rat    Sample: immunoreactive cells

Figure 6 Influence of spinal canal environment on western blot results after primary spinal cord injury in different groups at 7 days post-operation. (A) Western blot bands: The bands were more obvious in the SCIC group than in the SCIO group. (B) Percentage of objective protein expression in the injured spinal cord. The expression of HIF-1α and VEGF proteins was higher in the SCIC group than in the SCIO group (*P < 0.05; mean ± SD, n = 8; one-way analysis of variance followed by the Bonferroni correction in various groups). HIF-1α: Hypoxia-inducible factor 1α; SCIC: spinal cord injury with closed canal; SCIO: spinal cord injury with open canal; VEGF: vascular endothelial growth factor.

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