MA1-16629

antibody from Invitrogen Antibodies

Targeting: VEGFA VEGF, VEGF-A, VPF

Provider product page for MA1-16629

Western blot

ELISA

Antibody data

Antibody Data
Antigen structure
References [71]
Comments [0]
Validations
Western blot [3]
Immunocytochemistry [1]
Immunohistochemistry [1]
Flow cytometry [2]
Other assay [13]

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Product number: MA1-16629 - Provider product page
Provider: Invitrogen Antibodies
Product name: VEGF Monoclonal Antibody (VG1)
Antibody type: Monoclonal
Antigen: Recombinant full-length protein
Reactivity: Human, Mouse, Rat, Canine, Porcine
Host: Mouse
Isotype: IgG
Antibody clone number: VG1
Vial size: 100 µg
Concentration: 1 mg/mL
Storage: Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

VEGFA protein structure - MA1-16629 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 8 VEGF expression. Tissue samples were collected, decalcified and processed for immunohistochemistry at day 17 of the study. Staining intensity for VEGF based on the number of pixels associated with the DAB staining. The results are represented as mean +- standard deviation of eleven animals. One-way ANOVA with Tukey's multiple comparison test was used to assess intergroup differences ( ** P < 0.01, *** P < 0.001, **** P < 0.0001).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: FIGURE 7 Effects of IHH and IHH+LAE on (A) the biomarker of mitochondrial content citrate synthase activity and (B) the relative content of the pro-angiogenic factor VEGF in TA muscle homogenates. Band's intensity were normalized to the Ponceau staining and then relativized to the TNI group. * indicates P < 0.05 compared to TNI rats.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 11 Expression of VEGF at wound sites of nude mice in the IFS and IFS + SF groups 7 days after surgery, as revealed by immunohistochemical examination. The high-magnification images show a high density of microvessels (e, j). Scale bars, 200 mu m.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: FIGURE 2 Circ_CLASP2 overexpression promoted proliferation and inhibited apoptosis in HUVECs under HG conditions. (A) Circ_CLASP2 expression was assessed by qRT-PCR in HUVECs transfected with Vector or circ_CLASP2. HUVECs were transfected with Vector or circ_CLASP2 and then treated with HG, followed by the measurement of cell colony formation using a colony formation assay (B) , cell proliferation by MTT assay (C) , Ki67 level by Western blot (D) , cell apoptosis by flow cytometry (E) , Bcl-2, Bax and Cleaved PARP levels (F), and VEGF expression (G) by Western blot. Vector: negative control vector, circ_CLASP2: circ_CLASP2 overexpression vector. n = 3 independent biological replicates; data were presented as mean +- SD; * p < 0.05 by a two-tailed Student''s t -test or ANOVA followed by Tukey-Kramer post hoc test.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: FIGURE 4 Overexpression of circ_CLASP2 regulated proliferation and apoptosis of HG-treated HUVECs by miR-140-5p. (A) MiR-140-5p expression was tested by qRT-PCR in HUVECs transfected with Vector, circ_CLASP2, circ_CLASP2+miR-NC mimic, or circ_CLASP2+miR-140-5p mimic. HUVECs were transfected with Vector, circ_CLASP2, circ_CLASP2+miR-NC mimic, or circ_CLASP2+miR-140-5p mimic before HG treatment, followed by the determination of cell colony formation using a colony formation assay (B) , cell proliferation by MTT assay (C) , Ki67 level by Western blot (D) , cell apoptosis by flow cytometry (E) , Bcl-2, Bax and Cleaved PARP levels (F) , and VEGF expression (G) by Western blot. Vector: negative control vector, circ_CLASP2: circ_CLASP2 overexpression vector. n = 3 independent biological replicates; data were presented as mean +- SD; * p < 0.05 by ANOVA followed by Tukey-Kramer post hoc test.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: FIGURE 6 MiR-140-5p regulated HUVEC proliferation and apoptosis under HG conditions by FBXW7. (A,B) FBXW7 mRNA and protein levels were measured by qRT-PCR or Western blot assay in HUVECs transfected with anti-miR-NC, anti-miR-140-5p, anti-miR-140-5p + si-NC, or anti-miR-140-5p + si-FBXW7. HUVECs were transfected with anti-miR-NC, anti-miR-140-5p, anti-miR-140-5p + si-NC, or anti-miR-140-5p + si-FBXW7 before HG treatment, followed by the determination of cell colony formation using a colony formation assay (C) , cell proliferation by MTT assay (D) , Ki67 level by Western blot (E) , cell apoptosis by flow cytometry (F) , Bcl-2, Bax and Cleaved PARP levels (G) , and VEGF expression (H) by Western blot. * p < 0.05. n = 3 independent biological replicates; data were presented as mean +- SD; * p < 0.05 by ANOVA followed by Tukey-Kramer post hoc test.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 4 NOTCH2 plays a vital role in ECFC angiogenesis. PCR ( a ) and WB ( b ) analysis of the RNA and protein levels of NOTCH2, VEGF, and bFGF in ECFCs after NC and NOTCH2 inhibitor transfection. c ELISA analysis of VEGF secretion from ECFCs after transfection. Tube formation ( d , e ), Transwell ( f , g ), wound healing ( h , i ), and proliferation ( j ) assays revealed that inhibiting NOTCH2 impairs angiogenesis. k , l CAM angiogenesis assays revealed that when injected with ECFCs in which NOTCH2 was inhibiting, new chick embryo vessel density decreased. Data are means +- S.D. (N.S, no significance; # P > 0.05, * P < 0.05, ** P < 0.01, and *** P < 0.001; n = 3 independent experiments)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 5 MiR-205 regulates ECFC function via inhibiting NOTCH2. PCR ( a ) and WB ( b ) analyses of the RNA and protein levels of NOTCH2, VEGF, and bFGF in ECFCs after transfection with dual-NC, NOTCH2i-NC + miR-205i, or both inhibitors. c VEGF secretion from ECFCs after transfection was measured via ELISA. The results of proliferation ( d ), tube formation ( e , f ), Transwell ( g , h ), and wound healing ( i , j ) assays revealed that miR-205 was able to reverse the angiogenic activity that was impaired by NOTCH2 inhibitor. k , l Representative photographs of capillaries in CAM samples. Data are means +- S.D. (N.S, no significance; # P > 0.05, * P < 0.05, ** P < 0.01, and *** P < 0.001; n = 3 independent experiments)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 Immunohistochemistry scores for HSP70, pERK1/2 and VEGFA in both components of DDCS. Immunohistochemistry scores for WD and DD components where ERK = pERK1/2; HS = HSP70 and VG = VEGFA.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 2 HSP70, pERK1/2, and VEGFA Expression in Both Components of DDCS: A: H&E depicting both components of DDCS (100X) B: HSP70 immunohistochemistry in well differentiated component of dedifferentiated chondrosarcoma (400X); C: HSP70 immunohistochemistry in dedifferentiated component of dedifferentiated chondrosarcoma (400X); D: pERK1/2 in both components (400X); E: VEGFA immunohistochemistry in both components (400X).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 Immunoblotting for HIF1alpha and VEGF in the rat retina. A : Representative immunoblots for HIF1alpha and VEGF. B : Quantification of the corresponding densitometry data. The protein expression was normalized to the tubulin and was represented as %control. Data are mean +- standard error of the mean (SEM, n=3). C, control; D, diabetes; D+B12, diabetic rats treated with vitamin B 12 . *Significant difference from the control group; # significant difference from the diabetes group (p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: FIGURE 3 Methyltransferase-like 3 enhances PI3K/AKT signaling pathway activation and angiogenic cytokine production. (A) Gene Ontology enrichment analysis of the angiogenic targets of METTL3. (B) Following METTL3 knockdown or overexpression, the mRNA levels of the angiogenic cytokine VEGF were significantly altered. (C) PI3K/AKT signaling pathway and angiogenesis-related proteins including PI3Kp110, AKT, p-AKT, and VEGF were assessed via Western blotting in EPCs, with ImageJ being used for analysis. Analyses were conducted using data from three independent experiments. NC-OE and OE-METTL3 groups or NC-shRNA and METTL3-shRNA groups were compared via Student's t -tests. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001; n = 3 in each independent experiments.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: 4 FIGURE Citrulline ameliorates fibrosis and promotes angiogenesis in the placenta. l -Citrulline (2.5 g*L -1 in drinking water) was administered from the day of mating to the end of the experiments. At GD21, the placentas were fixed in formalin and embedded in paraffin. Placenta sections were stained using Masson's trichome staining kit, and the blue colour indicates positive stain for collagen. Magnification: 100x (a). Collagen staining was quantified using ImageJ software (b). n = 6 animals per group. The expression of remodelling genes, for TGF-beta ( Tgfb ) and MMP 2 and 9 ( Mmp2 and Mmp9 ), in the placenta was analysed by quantitative PCR (c). The expression of endothelial cell marker CD31 was examined by immunohistochemistry (IHC) staining using anti-CD31 antibody. Magnification: 100x (d). Black arrows indicate small vessels with positive stain. The expression of angiogenic ( Plgf , placental growth factor; Vegf , vascular endothelial growth factor; Fgf2 , fibroblast growth factor) and anti-angiogenic ( Flt-1 , fms-like tyrosine kinase 1; Thbs , thrombospondin; Angpt2 , angiopoietin 2; Lkb1 , liver kinase b1) genes in the placenta was measured by quantitative PCR (e). The protein expression of CD31 (f), placental growth factor (PlGF), and vascular endothelial growth factor (VEGF) (g) in the placenta was measured by Western blotting. beta-tubulin was used as internal control. Data are presented as means +- SEM, with individual values. * P < 0.05, significantly different