Vimentin Antibody - #AF7013

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Product: Vimentin Antibody
Catalog: AF7013
Description: Rabbit polyclonal antibody to Vimentin
Application: WB IHC IF/ICC
Cited expt.: WB, IHC, IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 53kDa; 54kD(Calculated).
Uniprot: P08670
RRID: AB_2835318

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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:200
*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(100%), Horse(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Vimentin Antibody detects endogenous levels of total Vimentin.
RRID:
AB_2835318
Cite Format: Affinity Biosciences Cat# AF7013, RRID:AB_2835318.
Conjugate:
Unconjugated.
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. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

CTRCT30; Epididymis luminal protein 113; FLJ36605; HEL113; VIM; VIME_HUMAN; Vimentin;

Immunogens

Immunogen:

A synthesized peptide derived from human Vimentin

Uniprot:

P08670(VIME_HUMAN) >>Visit HPA database.

Gene(ID):
VIM(7431)
Expression:
P08670 VIME_HUMAN:

Highly expressed in fibroblasts, some expression in T- and B-lymphocytes, and little or no expression in Burkitt's lymphoma cell lines. Expressed in many hormone-independent mammary carcinoma cell lines.

Description:
VIM is an intermediate filament protein. Intermediate filament proteins are expressed in a tissue-specific manner. Desmin is the subunit specific for muscle and vimentin the subunit specific for mesenchymal tissue.
Sequence:
MSTRSVSSSSYRRMFGGPGTASRPSSSRSYVTTSTRTYSLGSALRPSTSRSLYASSPGGVYATRSSAVRLRSSVPGVRLLQDSVDFSLADAINTEFKNTRTNEKVELQELNDRFANYIDKVRFLEQQNKILLAELEQLKGQGKSRLGDLYEEEMRELRRQVDQLTNDKARVEVERDNLAEDIMRLREKLQEEMLQREEAENTLQSFRQDVDNASLARLDLERKVESLQEEIAFLKKLHEEEIQELQAQIQEQHVQIDVDVSKPDLTAALRDVRQQYESVAAKNLQEAEEWYKSKFADLSEAANRNNDALRQAKQESTEYRRQVQSLTCEVDALKGTNESLERQMREMEENFAVEAANYQDTIGRLQDEIQNMKEEMARHLREYQDLLNVKMALDIEIATYRKLLEGEESRISLPLPNFSSLNLRETNLDSLPLVDTHSKRTLLIKTVETRDGQVINETSQHHDDLE

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
Horse
100
Bovine
100
Dog
100
Xenopus
100
Chicken
100
Rabbit
100
Zebrafish
73
Sheep
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Vimentins are class-III intermediate filaments found in various non-epithelial cells, especially mesenchymal cells. Vimentin is attached to the nucleus, endoplasmic reticulum, and mitochondria, either laterally or terminally.

Involved with LARP6 in the stabilization of type I collagen mRNAs for CO1A1 and CO1A2.

PTMs:

Filament disassembly during mitosis is promoted by phosphorylation at Ser-55 as well as by nestin (By similarity). One of the most prominent phosphoproteins in various cells of mesenchymal origin. Phosphorylation is enhanced during cell division, at which time vimentin filaments are significantly reorganized. Phosphorylation by PKN1 inhibits the formation of filaments. Phosphorylated at Ser-56 by CDK5 during neutrophil secretion in the cytoplasm. Phosphorylated by STK33. Phosphorylated on tyrosine residues by SRMS.

O-glycosylated during cytokinesis at sites identical or close to phosphorylation sites, this interferes with the phosphorylation status.

S-nitrosylation is induced by interferon-gamma and oxidatively-modified low-densitity lipoprotein (LDL(ox)) possibly implicating the iNOS-S100A8/9 transnitrosylase complex.

Subcellular Location:

Cytoplasm. Cytoplasm>Cytoskeleton. Nucleus matrix.

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

Highly expressed in fibroblasts, some expression in T- and B-lymphocytes, and little or no expression in Burkitt's lymphoma cell lines. Expressed in many hormone-independent mammary carcinoma cell lines.

Family&Domains:

The central alpha-helical coiled-coil IF rod domain mediates elementary homodimerization.

The [IL]-x-C-x-x-[DE] motif is a proposed target motif for cysteine S-nitrosylation mediated by the iNOS-S100A8/A9 transnitrosylase complex.

Belongs to the intermediate filament family.

Research Fields

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

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

References

1). Genomic and Transcriptomic Characterization of Natural Killer T Cell Lymphoma. CANCER CELL, 2020 (PubMed: 32183952) [IF=48.8]

Application: IF/ICC    Species: human    Sample: NK-92 cells

Figure 6. Biological Function of MGA and BRDT. (D) Immunofluorescence images of E-cadherin (green), fibronectin (red), or vimentin (red) in NK-92 cells transfected with MGA shRNAs or scramble. Cells were counterstained with DAPI (blue). (G) Immunofluorescence images of E-cadherin (green), fibronectin (red), or vimentin (red) in NK-92 cells transfected with pCMV6-BRDT (upper panel) or vector control (lower panel). Cells were counterstained with DAPI (blue).
2). CircGPR137B/miR-4739/FTO feedback loop suppresses tumorigenesis and metastasis of hepatocellular carcinoma. Molecular Cancer, 2022 (PubMed: 35858900) [IF=37.3]

Application: WB    Species: Human    Sample: HepG2 and Hep3B cells

Fig. 6 FTO is regulated by circGPR137B/miR-4739 axis in HCC. A Schematic representation of the binding sites between miR-4739 and FTO 3’UTR. B Comparison of the luciferase activity of WT or Mut FTO 3’UTR after treatment with miR-4739 mimics in HepG2 and Hep3B cells. C, D RT-qPCR and western blot analysis of the expression of FTO, p21, p27, cleaved caspase-3/− 9, N-cadherin, E-cadherin and vimentin after the transfection with circGPR137B lentiviruses and (or) miR-4739 mimics in HepG2 and Hep3B cells. E, F, G MTT, colony formation and transwell analysis of the cell proliferation, colony number and cell invasion after the transfection with FTO plasmids and (or) miR-4739 mimics in HepG2 and Hep3B cells. Data are the means ± SEM of three experiments. *P < 0.05, **P < 0.01, ***P < 0.001
3). A novel UV-curable extravascular stent to prevent restenosis of venous grafts. Composites Part B: Engineering, 2021 [IF=12.7]

Application: WB    Species: Rat    Sample:

Fig. 6. A: PCNA immunofluorescence staining of venous graft vessels in rats. B, C: Western blot analysis of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. D: ICAM-1 immunofluorescence staining of venous graft vessels in rats. E: qPCR of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. Data are presented as the mean ± SD; *: compared with control group, p < 0.05. #: compared with sham group,
4). YY1 complex promotes Quaking expression via super-enhancer binding during EMT of hepatocellular carcinoma. CANCER RESEARCH, 2019 (PubMed: 30760518) [IF=12.5]

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

Fig. 3| YY1 and p65 promote EMT, migration, and invasion by targeting QKI. (a) Expression of E-cadherin and Vimentin transfected with YY1, p65, and QKI or co-transfected with QKI siRNA.

Application: IF/ICC    Species: human    Sample: PLC-PRF-5 cells

Fig. 3| YY1 and p65 promote EMT, migration, and invasion by targeting QKI. (a) Expression of E-cadherin and Vimentin transfected with YY1, p65, and QKI or co-transfected with QKI siRNA. (b) Morphological changes in PLC-PRF-5 cells transfected with YY1, p65, and QKI or co-transfected with QKI siRNA observed with SEM. (c) Representative immunofluorescence images of E-cadherin and Vimentin of PLC-PRF-5 cells treated in the same manner as in the wound-healing assay.

Application: IHC    Species: mouse    Sample: tumor tissues

Fig. 5| QKI expression is required for the YY1 complex to promote the metastasis and malignancy of HCC. (a) Comparison of PLC-PRF-5 and Hep3B tumor growth in mice were measured starting 6 days after implantation. All of the groups were euthanized on day 24. (b) Metastatic lung nodules were counted in each group. (c) QKI, p65, YY1, E-cadherin, and Vimentin expression levels in the tumor tissues of p65, YY1, p65+YY1, QKI and p65+YY1+siQKI groups analyzed through IHC staining.
5). Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma. CANCER RESEARCH, 2018 (PubMed: 29844124) [IF=12.5]

Application: IF/ICC    Species: human    Sample: PLC cells

Figure 3. |Twist1 up-regulates Vimentin expression through increased circ-10720,which adsorbs miRNA.(F) Representative immunofluorescence images of Ecadherin and Vimentin in PLC cells transfected with Twist1 alone or co-transfected with circ-10720 siRNA.

Application: WB    Species: human    Sample: PLC cells

Figure 3. |Twist1 up-regulates Vimentin expression through increased circ-10720,which adsorbs miRNA.(E) The expression level of Vimentin was measured by western blot in PLC cells transfected with Twist1 alone or co-transfected with circ10720 siRNA. Intensity of each band from biological triplicate experiments was quantified by densitometry with the Image J software with GAPDH as a normalizer.**P<0.01, one-way ANOVA.

Application: IHC    Species: human    Sample: tumor

Figure 4. |Intratumoral silencing of circ-10720 blocks the promotive effect of Twist1-mediated on Vimentin expression in a PDTX model of HCC. (E, F) Twist1 and Vimentin expression in the tumor tissues of Twi-L+control, Twi-L+circ-10720, Twi-H+siRNA control and TwiH+si-circ-10720 groups were analyzed via IHC. Each bar represents the mean ± SD for triplicate measurements of four xenografts in each group. **P<0.01, one-way ANOVA.
6). Combination therapy of PKCζ and COX-2 inhibitors synergistically suppress melanoma metastasis. Journal of Experimental & Clinical Cancer Research, 2017 (PubMed: 28865485) [IF=11.3]

Application: WB    Species: mouse    Sample: B16F10

Fig. 5 The expression of p-PKCζ, p-cofilin and COX-2 after combined treatment of J-4 and Celecoxib. (a) Western blotting images of p-cofilin and COX-2 in B16-F10 cells with various treatments for 24 h. (b) Western blotting images of p-cofilin and COX-2 in A375 cells with various treatments for 24 h. (c) Relative mRNA level of PKCζ and COX-2 determined via RT-PCR. (d) The expression of EMT markers, E-Cadherin and Vimentin, and MMP-2/MMP-9 was affected in B16-F10 and A375 cells after various treatments for 24 h. J-4: 25 μM; Celecoxib: 25 μM. * P < 0.05; ** P < 0.01
7). Stearoyl-CoA desaturase-1 promotes colorectal cancer metastasis in response to glucose by suppressing PTEN. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2018 (PubMed: 29530061) [IF=11.3]

Application: WB    Species: human    Sample: CRC

Fig. 2| SCD1 promotes migration and invasion of colorectal cancer cells by regulating EMT. i, j Protein levels of E-cadherin and vimentin in colorectal cancer cells transfected with SCD1 shRNA (i) or SCD1 cDNA (j)
8). Lactate drives epithelial-mesenchymal transition in diabetic kidney disease via the H3K14la/KLF5 pathway. Redox biology, 2024 (PubMed: 38925041) [IF=10.7]

Application: WB    Species: Mouse    Sample:

Fig. 4. Sodium oxamate (Ox), an LDHA inhibitor, attenuates EMT in db/db mice. (A) Experiment design. (B) The content of lactate acid. (C–F) The level of glucose, ALB, BUN, and Scr. (G–K) The protein expression level of E-cadherin, ZO-1, Vimentin, and ɑ-SMA. vel of glucose, ALB, BUN, and Scr. (G–K) The protein expression level of E-cadherin, ZO-1, Vimentin, and ɑ-SMA. (L–N) Immunofluorescent staining of E-cadherin (red), ɑ-SMA (green), and DAPI (blue). Scale bars, 50 μm. (O–P) Masson's trichrome stain. Scale bars, 20 μm. All statistic data were presented as mean ± SEM. n = 6, Two-way ANOVA followed by Tukey'smultiple comparisons test. All tests were two tailed. Data are expressed as Mean ± SEM, #P < 0.05, ##P < 0.01; *P < 0.05, **P < 0.01. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
9). Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107. CANCER LETTERS, 2021 (PubMed: 33160003) [IF=9.1]

Application: WB    Species: Human    Sample: HNE1 and 5–8F cell

Fig. 2. miR-107 promotes nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro. a CCK-8 assays were conducted after transfection with miR-107 mimics or inhibitors in HNE1 and 5–8F cell lines. b Colony-forming capacity was determined after transfection with miR-107 mimics or inhibitors in HNE1 and 5–8F cell lines. c Migratory potential was examined in cells transfected with miR-107 mimics or inhibitors by wound healing assay. d Invasive potential of cells was examined in cells transfected with miR-107 mimics or inhibitors using Transwell chambers with Matrigel. e Apoptosis was evaluated using cells transfected with miR-107 mimics or inhibitors. f Protein markers of EMT (E-cadherin, N-cadherin, and vimentin) were detected by Western blot analysis after transfection with miR-107 mimics or inhibitors in HNE1 and 5–8F cell lines. The values are expressed as the mean ± SD of three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.
10). Protopanaxadiol inhibits epithelial-mesenchymal transition of hepatocellular carcinoma by targeting STAT3 pathway. Cell Death & Disease, 2019 (PubMed: 31431619) [IF=8.1]

Application: WB    Species: human    Sample: PLC/PRF/5 and HepG2 cells

Fig. 4 | PPD inhibited EMT of HCC cells by targeting STAT3. Protein expression level changes of Twist1, E-cadherin, and vimentin in the PLC/PRF/5 and HepG2 cells treated with PPD.The GAPDH blot served as a loading contro

Application: IF/ICC    Species: human    Sample: PLC/PRF/5 and HepG2 cells

Fig. 3 |PPD inhibited the invasion and EMT of the PLC/PRF/5 and HepG2 cells. a PPD inhibited the invasion ability of PLC/PRF/5 and HepG2 cells.b PPD inhibits the colony forming ability of hepatoma cell lines. c Typical images of immunofluorescent double staining for E-cadherin and vimentin in PLC/PRF/5 and HepG2 cells treated with PPD.
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