MA5-11883

antibody from Invitrogen Antibodies

Targeting: VIM

Provider product page for MA5-11883

Western blot

Immunocytochemistry

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [244]
Comments [0]
Validations
Western blot [1]
Immunocytochemistry [2]
Immunohistochemistry [2]
Other assay [21]

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Product number: MA5-11883 - Provider product page
Provider: Invitrogen Antibodies
Product name: Vimentin Monoclonal Antibody (V9)
Antibody type: Monoclonal
Antigen: Purifed from natural sources
Description: MA5-11883 targets Vimentin in IHC (P) applications and shows reactivity with Bovine, Canine, Chicken, Equine, Feline, Gerbil, Hamster, Human, mouse, Non-human primate, Porcine, Rabbit, and Rat samples.
Antibody clone number: V9
Concentration: 0.5 mg/mL

VIM protein structure - MA5-11883 shown in red.

Supportive validation

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Experimental details: Immunofluorescent analysis of Vimentin (green) in HeLa cells. The cells were fixed with 4% paraformaldehyde for 15 minutes, permeabilized with 0.1% Triton X-100 in PBS for 15 minutes, and blocked with 3% Blocker BSA (Product # 37525) in PBS for 30 minutes at room temperature. Cells were stained with a Nucleophosmin monoclonal antibody (Product # MA5-11883) at a concentration of 10 µg/mL for 1 hour at room temperature, and then incubated with a Goat anti-Mouse IgG (H+L) Superclonal Secondary Antibody, Alexa Fluor® 488 conjugate (Product # A28175) at a dilution of 1:1000 for 1 hour at room temperature (green). Nuclei (blue) were stained with Hoechst 33342 dye (Product # 62249). Images were taken on a Thermo Scientific ToxInsight at 20X magnification.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunofluorescence analysis of Vimentin was performed using 70% confluent log phase NIH/3T3 cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 10 minutes, and blocked with 1% BSA for 1 hour at room temperature. The cells were labeled with Vimentin (V9) Mouse Monoclonal Antibody (Product # MA5-11883) at 2 µg/mL in 0.1% BSA and incubated for 3 hours at room temperature and then labeled with Goat anti-Mouse IgG (H+L) Superclonal™ Secondary Antibody, Alexa Fluor® 488 conjugate (Product # A28175) at a dilution of 1:2000 for 45 minutes at room temperature (Panel a: green). Nuclei (Panel b: blue) were stained with SlowFade® Gold Antifade Mountant with DAPI (Product # S36938). F-actin (Panel c: red) was stained with Rhodamine Phalloidin (Product # R415, 1:300). Panel d represents the merged image showing cytoplasmic localization. Panel e shows the no primary antibody control. The images were captured at 60X magnification.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunoprecipitation of Vimentin using Vimentin Monoclonal Antibody (Product # MA5-11883) on denatured Human HeLa Cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunoprecipitation of Vimentin using Vimentin Monoclonal Antibody (Product # MA5-11883) on Native Human HUVEC Cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 2 Snail suppresses tumor progression and is associated with tumor immunity. a Western blot of HM-1-control and HM-1-shSnail cells. CDH1: E-Cadherin, VIM vimentin. b Invasion of HM-1-control and HM-1-shSnail cells; n = 5. c Wound healing of HM-1-control and HM-1-shSnail cells. Data represent the percentage of wound width (24 h) relative to that at 0 h; n = 6. d Growth curves of HM-1-control and HM-1-shSnail subcutaneous tumors in immunocompetent mice. P -values represent significance between two groups at day 31; n = 6. e Growth curves of HM-1-control and HM-1-shSnail subcutaneous tumors from immunodeficient nude mice; n = 6; NS no significant difference between two groups at day 23. * P < 0.05, ** P < 0.01, and *** P < 0.001 (one-way ANOVA with Tukey's multiple comparisons test in b - e ). Averaged data are presented as the mean +- SEM

Supportive validation

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Experimental details: Figure 5 UVRAG FS activates Rac-1 and promotes tumour metastasis in vitro and vivo . ( a ) Rac-1 activation by UVRAG FS . Western blot shows a pull-down experiment to detect GTP-bound Rac1 in SW480.UVRAG FS cells and on drug treatment. Histogram shows quantification from three independent experiments. ( b ) Representative images of scratch-wound healing exhibit the motility of SW480.UVRAG FS cells. Cell motility into the wound area was taken at 0 and 16 h as marked by red lines. Wound-healing index was quantified (right). Data are the means+-s.d. ( n =3). ** P

Supportive validation

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Experimental details: Figure 1 Immunofluorescence localization of NCOA6 in the first- and second-trimester human placental tissues. NCOA6 staining was observed in the CTBs, STBs, TC and EVTs but not in the villous MCs of normal first-trimester and second-trimester placentas (A-J). NCOA6 staining was also found in uterine SCs (K, L). In the representative images of a first-trimester placental villus from the 6th week of gestation (A-F), NCOA6 was highly expressed in the TC (C, D). In the representative images of a second-trimester placenta from the 20th week of gestation (G-L), strong expression of NCOA6 in the nucleus of EVTs was found (I, J). CK7 was used as the marker for placental trophoblasts; HLA-G was used as the marker for EVTs; and Vimentin was used as the marker for villous MCs and uterine SCs. Scale bars: 50 mum. CTBs indicates cytotrophoblasts; EVTs, extravillous trophoblasts; HLA-G, human leucocyte antigen-G; MCs, mesenchymal cells; SCs, stromal cells; STBs, syncytiotrophoblasts; TC, trophoblast column

Supportive validation

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Experimental details: Fig. 1 miR-17-5p is inversely correlated with the expression of vimentin in colon cancer cells. a miR-17-5p expression was lower in primary CRC tissues with metastasis compared with primary CRC tissues without metastasis ( p = 0.002). b The cells were harvested and subsequently analysed for the differential expression of proteins by western blot. beta-actin was used as the loading control. E-cadherin and vimentin were used in western blotting analysis. c The expression of vimentin was negatively correlated with that of miR-17-5p in clinical specimens. d The expression of miR-17-5p and vimentin was examined in CRC cell lines by qRT-PCR. The miR-17-5p was inversely correlated with vimentin expression.

Supportive validation

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Experimental details: Figure 2. miR-939-3p promotes invasion and EMT in a HCC cell line. (A) Transfection efficiency of miR-939-3p mimic and inhibitor was detected by reverse transcription quantitative PCR. *P

Supportive validation

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Experimental details: Figure 2 TGF-beta-induced cell migration and invasion was reversed by knockdown of TAGLN . ( A ) Cell migration and invasion in HCT116 cells (left panel) and representative images of crystal violet staining (right panel). ( B ) Cell migration and invasion in HT29 cells (left panel) and representative images of crystal violet staining (right panel). ( C ) Representative images of Western blotting assay of E-cadherin, vimentin, fibronectin, MMP2, MMP9, and GADPH . 200 x magnification. * P

Supportive validation

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Experimental details: Figure 4 Overexpression of HMGA2 restored altered CRC cell migration and invasion induced by inhibition of TAGLN . ( A ) Cell migration and invasion in HCT116 cells (left panel) and representative images of crystal violet staining (right panel). ( B ) Cell migration and invasion in HT29 cells (left panel) and representative images of crystal violet staining (right panel). ( C ) Representative images of Western blotting assay of nucleus and total TAGLN levels. ( D ) Representative images of Western blotting assay of E-cadherin, vimentin, fibronectin, MMP2, MMP9, and GADPH . 200 x magnification. * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 TGF-beta-induced TAGLN expression increased migration and invasion of tumor promoting. ( A ) Image of tumors in nude mice inoculated with HT29 cells (Blank) and HT29 cells pretreated with TGF-beta and si- TAGLN (TGF-beta+si- TAGLN group). ( B ) Tumor volume was measured every four days. Tumor volume=1/2*L*W*W. * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 7 ZO-2 associates to SUN-1 and lamin B1, and its absence triggers an increased expression of SUN-1 and nesprins-3, and -4 and reduces vimentin. ( a ) Western blot detection of nesprins-3 and -4 in parental and ZO-2 KD cells transfected or not with hZO-2. Upper panels, representative images; lower panels, quantitative analysis obtained from three independent experiments. GAPDH is used as a loading control. Statistical analysis was done with One-way ANOVA followed by Tukey's multiple comparisons test. Results shown as media +- standard deviation, * p < 0.05, ** p < 0.01, *** p < 0.001. ( b ) Left panel, representative immunofluorescence images showing ZO-2 and vimentin expression in parental and ZO-2 KD cells transfected or not with hZO-2. Bar, 20 mum. Right panel, representative Western blot of three independent experiments and corresponding quantitative analysis. GAPDH is used as a loading control. Statistical analysis was done with One-way ANOVA followed by Tukey's multiple comparisons test. Results are shown as media +- standard deviation, **** p < 0.0001; ns, non-significant. ( c ) Western blot detection of SUN-1 in parental and ZO-2 KD cells transfected or not with hZO-2. Upper panel, representative image; lower panel, quantitative analysis obtained from three independent experiments. GAPDH is used as a loading control. Statistical analysis was done with One-way ANOVA followed by Tukey's multiple comparisons test. Results are shown as media +- standard deviation, *

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 6 Hypoxia induces the STAT3/miR-19a/PTEN axis to affect activity of the CRC cells: (a) proliferation and viability of cells examined by the CCK-8 assay ( * #& p < 0.05, two-way ANOVA); (b, c) migration (b) and invasion (c) of cells examined by Transwell assays ( * #& p < 0.05, two-way ANOVA); (d) protein levels of E-cadherin and Vimentin in HCT116 and SW480 cells examined by western blot analysis ( * #& p < 0.05, two-way ANOVA). Data were presented as the mean +- SD from three independent experiments. * Compared to the hypoxia + STAT3-NC group; # compared to the si-STAT3 + miR-19a control group; & compared to the miR-19a mimic + PTEN-NC group.

Supportive validation

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Experimental details: Immunohistochemical staining of vimentin in the chicken esophageal wall. (A) Vimentin + TCs in the subepithelium of the chicken esophageal wall; (B) vimentin + TCs around the mucosal glands of the chicken esophageal wall; (C) vimentin + TCs scattered throughout the lamina propria of the chicken esophageal wall; (D) vimentin was present in the blood vessels in the esophageal wall. Ep, epithelium; LP, lamina propria; MG, mucosal gland; BV, blood vessel. Black arrow = vimentin + TCs. Scale bar: 20 um. Figure 3

Supportive validation

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Experimental details: 7 FIGURE CBR1 (CBR1-green) confocal microscopic results, showing images of equine primary skin-derived cultures of keratinocytes (A-H) and fibroblasts (I-P). CBR1 immunoreactivity in keratinocytes (A and E) and fibroblasts (I and M). For keratinocyte and fibroblast immunophenotyping, co-labeling of CBR1 with specific epithelial pan-cytokeratin (CK-red) (B) and fibroblast vimentin (Vim-red) (N) markers was performed (yellow arrows indicate double positive cells). Inverse staining of Vim-red on keratinocytes (F) and CK-red on fibroblast (J) with CBR1 was additionally performed to distinguish both primary cell types (gray arrows indicate single positive cells). The DAPI (blue) was used for cell nucleus counterstaining; images were taken under 40x magnification; scale bars = 20 mum

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: 8 FIGURE CBR2 (CBR2-green) confocal microscopic results, showing images of equine primary skin-derived cultures of keratinocytes (A-H) and fibroblasts (I-P). CBR2 immunoreactivity in keratinocytes (A and E) and fibroblasts (I and M). For keratinocyte and fibroblast immunophenotyping, co-labeling with specific epithelial pan-cytokeratin (CK-red) (B) and fibroblast vimentin (Vim-red) (N) markers was performed (yellow arrows indicate double positive cells). In turn, inverse staining of Vim-red on keratinocytes (F) and CK-red on fibroblast (J) was additionally performed to distinguish both primary cell types (gray arrows indicate single positive cells). The DAPI (blue) was used for cell nucleus counterstaining; images were taken under 40x magnification; scale bars = 20 mum

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4 YTHDC1 is essential for TGF-beta-mediated EMT. A-B) Transwell migration and invasion assays for (A) MDA-MB-231 YTHDC1 KO cells (5x10 4 cells/well incubated for 5 hours for migration and 24 hours for invasion) or (B) SUM159 YTHDC1 KD cells (5x10 4 cells/well incubated for 24 hours for migration and invasion) treated with 5 ng/ml TGF-beta. One-way ANOVA compared to sgNS (MDA-MB-231) or shNS (SUM159) group. * P < 0.05. C-D) Western Blot for protein quantification from (C) MDA-MB-231 YTHDC1 KO cells or (D) SUM159 YTHDC1 KD cells treated with 5 ng/ml TGF-beta for 24 hours. E-F) RT-qPCR of TGF-beta responsive genes in (E) MDA-MB-231 YTHDC1 KO cells or (F) SUM159 YTHDC1 KD cells treated with 5 ng/ml TGF-beta for 24 hours. One-way ANOVA compared to sgNS (MDA-MB-231) or shNS (SUM159) group. * P < 0.05. G) Western Blot for protein quantification from HCC1806 YTHDC1 KD cells treated with 5 ng/ml TGF-beta for 72 hours. H) RT-qPCR of TGF-beta responsive genes in HCC1806 YTHDC1 KD cells treated with 5 ng/ml TGF-beta for 72 hours. One-way ANOVA compared to shNS group. NS = not significant, * P < 0.05. I) Images and quantification of the shapes of control, YTHDC1 MDA-MB-231 KO and SUM159 KD cells treated with TGF-beta or vehicle control for 4 days and stained with vimentin. Scale bar: 50 mum. A larger aspect ratio represents a more elongated cell shape. One-way ANOVA compared to control shNS group. NS = not significant, * P < 0.05.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 Changes in cell morphology and gene expression under hypoxia. ( A ) Immunofluorescent staining (red) of the epithelial marker E-cadherin (HECD-1) and the mesenchymal marker vimentin (V9). Three human breast cell lines, MDA-MB-231, MCF-7, and MCF-10A cells were cultured in hypoxia for 72 h prior to staining. The secondary antibody is rabbit anti-mouse labelled with AlexaFluor 594. Cell nuclei were stained with DAPI. Relative fluorescence intensity of ( B ) E-Cadherin and ( C ) vimentin. Cells were cultured in normoxic and hypoxic conditions for 72 hours prior to the staining. Mean +- S.E.M. data are shown (n = 3); ** p < 0.01 (Student's t test). Scale bar is 100 um.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1. Expression of different markers in the eight human colon cancer cell lines analyzed. (A) Western blot analysis of EpCAM, LGR5, CD26, E-cadherin and vimentin expression in total cell extracts from the eight cell lines (20 mug of protein in each line). Data shown are representative of three experiments. (B) E-cadherin and EpCAM expression analysis by immunofluorescence in HT-29 and Caco-2 cells. (C) CD44 and CD26 expression analysis by immunofluorescence in HT-29 and Caco-2 cells. (D) LGR5 expression analysis by immunofluorescence in DLD-1 and Caco-2 cells. Nuclei were stained with DAPI. Scale bars: 50 mum.