Product: Vimentin Antibody
Catalog: AF7013
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 53kD; 54kD(Calculated).
Uniprot: P08670
RRID: AB_2835318

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Product Info

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

PTMs - P08670 As Substrate

Site PTM Type Enzyme
S2 Phosphorylation
T3 Phosphorylation
R4 Methylation
S5 Phosphorylation P17252 (PRKCA)
S7 O-Glycosylation
S7 Phosphorylation P17252 (PRKCA) , Q96GD4 (AURKB) , Q02156 (PRKCE) , P17612 (PRKACA)
S8 Phosphorylation P17252 (PRKCA)
S9 Phosphorylation P17252 (PRKCA)
S10 Phosphorylation P17252 (PRKCA)
Y11 Phosphorylation
R12 Methylation
R13 Methylation
T20 Phosphorylation
S22 Phosphorylation
R23 Methylation
S25 Phosphorylation P17252 (PRKCA) , Q96GD4 (AURKB) , P17612 (PRKACA)
S26 Phosphorylation Q13153 (PAK1) , P17252 (PRKCA) , Q13177 (PAK2)
S27 Phosphorylation
R28 Methylation
S29 Phosphorylation
Y30 Phosphorylation
T32 Phosphorylation
T33 O-Glycosylation
T33 Phosphorylation
S34 O-Glycosylation
S34 Phosphorylation P17252 (PRKCA)
T35 Phosphorylation
R36 Methylation
T37 Phosphorylation
Y38 Phosphorylation
S39 Phosphorylation P49137 (MAPKAPK2) , Q13177 (PAK2) , P17612 (PRKACA) , O75116 (ROCK2) , P31749 (AKT1) , Q13153 (PAK1) , Q96GD4 (AURKB) , P17252 (PRKCA)
S42 Phosphorylation P17252 (PRKCA)
R45 Methylation
S47 Phosphorylation P17612 (PRKACA) , Q96GD4 (AURKB)
T48 Phosphorylation
S49 Phosphorylation
R50 Methylation
S51 Phosphorylation Q13177 (PAK2) , Q13153 (PAK1) , P49137 (MAPKAPK2)
Y53 Phosphorylation
S55 O-Glycosylation
S55 Phosphorylation P24941 (CDK2) , P06493 (CDK1)
S56 Phosphorylation P78527 (PRKDC) , P06493 (CDK1) , P49137 (MAPKAPK2) , Q13153 (PAK1) , P24941 (CDK2) , Q00535 (CDK5)
Y61 Phosphorylation
T63 Phosphorylation
R64 Methylation
S65 Phosphorylation Q96GD4 (AURKB)
S66 Phosphorylation Q96GD4 (AURKB) , Q13177 (PAK2) , Q13153 (PAK1)
R69 Methylation
R71 Methylation
S72 Phosphorylation P17612 (PRKACA) , Q96GD4 (AURKB) , Q13464 (ROCK1) , O75116 (ROCK2)
S73 Phosphorylation Q13177 (PAK2) , Q96GD4 (AURKB) , P17612 (PRKACA) , Q13153 (PAK1)
S83 Phosphorylation Q13557 (CAMK2D) , Q9UQM7 (CAMK2A) , P49137 (MAPKAPK2) , P53350 (PLK1)
S87 Phosphorylation Q96GD4 (AURKB)
K97 Ubiquitination
T99 Phosphorylation
T101 Phosphorylation
K104 Acetylation
K104 Ubiquitination
R113 Methylation
Y117 Phosphorylation
K120 Acetylation
K120 Methylation
K120 Ubiquitination
K129 Acetylation
K129 Ubiquitination
K139 Acetylation
K139 Ubiquitination
K143 Ubiquitination
S144 Phosphorylation
Y150 Phosphorylation
R158 Methylation
K168 Acetylation
K168 Ubiquitination
R184 Methylation
K188 Ubiquitination
T202 Phosphorylation
S205 Phosphorylation
S214 Phosphorylation
K223 Ubiquitination
S226 Phosphorylation
K235 Acetylation
K235 Ubiquitination
K236 Acetylation
K236 Ubiquitination
S261 Phosphorylation
K262 Ubiquitination
T266 Phosphorylation
Y276 Phosphorylation
S278 Phosphorylation
K282 Acetylation
K282 Ubiquitination
Y291 Phosphorylation
K292 Acetylation
K292 Ubiquitination
K294 Acetylation
K294 Ubiquitination
S299 Phosphorylation
R310 Methylation
K313 Acetylation
K313 Sumoylation
K313 Ubiquitination
S316 Phosphorylation
T317 Phosphorylation
S325 Phosphorylation
T327 Phosphorylation
C328 S-Nitrosylation
K334 Acetylation
K334 Ubiquitination
T336 Phosphorylation
S339 Phosphorylation
Y358 Phosphorylation
T361 Phosphorylation
K373 Acetylation
K373 Ubiquitination
R381 Methylation
Y383 Phosphorylation
Y400 Phosphorylation
R401 Methylation
K402 Acetylation
K402 Sumoylation
K402 Ubiquitination
S409 Phosphorylation
R410 Methylation
S412 Phosphorylation
S419 Phosphorylation
S420 Phosphorylation
T426 Phosphorylation
S430 Phosphorylation P78527 (PRKDC)
T436 Phosphorylation
S438 Phosphorylation
K439 Acetylation
K439 Ubiquitination
T441 Phosphorylation
K445 Acetylation
K445 Methylation
K445 Sumoylation
K445 Ubiquitination
T446 Phosphorylation
T449 Phosphorylation
T458 Phosphorylation P00540 (MOS)
S459 Phosphorylation P78527 (PRKDC) , P53350 (PLK1) , P00540 (MOS)

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.

Subunit Structure:

Homopolymer assembled from elementary dimers. Interacts with LGSN and SYNM. Interacts (via rod region) with PLEC (via CH 1 domain) (By similarity). Interacts with SLC6A4. Interacts with STK33. Interacts with LARP6. Interacts with RAB8B (By similarity). Interacts with TOR1A; the interaction associates TOR1A with the cytoskeleton. Interacts with TOR1AIP1. Interacts with BCAS3. Interacts with DIAPH1. Identified in complexes that contain VIM, EZR, AHNAK, BFSP1, BFSP2, ANK2, PLEC, PRX and spectrin (By similarity). Interacts with EPPK1; interaction is dependent of higher-order structure of intermediate filament. Interacts with the non-receptor tyrosine kinase SRMS; the interaction leads to phosphorylation of VIM. Interacts with NOD2. Interacts (via head region) with CORO1C (By similarity). Interacts with HDGF (isoform 2).

(Microbial infection) Interacts with HCV core protein.

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). Xiong J et al. Genomic and Transcriptomic Characterization of Natural Killer T Cell Lymphoma. Cancer Cell 2020 Mar 16;37(3):403-419 (PubMed: 32183952) [IF=38.585]

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). Meng J et al. Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma. Cancer Res 2018 Aug 1;78(15):4150-4162 (PubMed: 29844124) [IF=13.312]

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.

3). Han J et al. YY1 complex promotes Quaking expression via super-enhancer binding during EMT of hepatocellular carcinoma. Cancer Res 2019 Feb 13 (PubMed: 30760518) [IF=13.312]

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.

4). Li W et al. Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107. Cancer Lett 2021 Feb 28;499:301-313. (PubMed: 33160003) [IF=9.756]

5). Yang L et al. Protopanaxadiol inhibits epithelial-mesenchymal transition of hepatocellular carcinoma by targeting STAT3 pathway. Cell Death Dis 2019 Aug 20;10(9):630 (PubMed: 31431619) [IF=9.685]

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.

6). Meng J et al. Hsp90β promotes aggressive vasculogenic mimicry via epithelial-mesenchymal transition in hepatocellular carcinoma. Oncogene 2018 Aug 7 (PubMed: 30087438) [IF=8.756]

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). Ran H et al. Stearoyl-CoA desaturase-1 promotes colorectal cancer metastasis in response to glucose by suppressing PTEN. J Exp Clin Cancer Res 2018 Mar 12;37(1):54 (PubMed: 29530061) [IF=7.068]

8). Ran H et al. Stearoyl-CoA desaturase-1 promotes colorectal cancer metastasis in response to glucose by suppressing PTEN. J Exp Clin Cancer Res 2018 Mar 12;37(1):54 (PubMed: 29530061) [IF=7.068]

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)

9). Song X et al. Microbial metabolite deoxycholic acid promotes vasculogenic mimicry formation in intestinal carcinogenesis. Cancer Sci 2022 Feb;113(2):459-477. (PubMed: 34811848) [IF=6.518]

10). Wang H et al. Oleanolic acid inhibits epithelial-mesenchymal transition of hepatocellular carcinoma by promoting iNOS dimerization. Mol Cancer Ther 2018 Oct 8 (PubMed: 30297361) [IF=6.009]

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

Figure 3. |OA inhibits EMT in HCC through unregulated E-cadherin expression and downregulated vimentin expression.(B) Immunofluorescence assay conducted in the HepG2 cancer cell line demonstrated that Downloaded from mct.aacrjournals.org on October 10, 2018. © 2018 American Association for Cancer Research. Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Author Manuscript Published OnlineFirst on October 8, 2018; DOI: 10.1158/1535-7163.MCT-18-0448 22 OA can enhance fluorescence intensity of E-cadherin and attenuate that of vimentin, whereas treatment of NO scavenger (C-PTIO) or transfection of siRNA iNOS exhibits the opposite effect. This outcome is consistent with the finding of Western blot assay. The results were obtained from three independent experiments, each performed in triplicate. Data are represented as mean ± standard error of the mean (*P < 0.05, **P < 0.01).

Application: IHC    Species: human    Sample: PLC cells

Figure 5. |OA exhibits anti-EMT effect in vivo and enhances the antitumor effect of regorafenib. (F) Results of IHC assays. The expression levels of E-cadherin were significantly upregulated, whereas those of vimentin, MMP2, and MMP9 were downregulated by OA or regorafenib treatment, and OA enhanced the effects of regorafenib. The expression levels of iNOS and NT were upregulated by OA but not by regorafenib. (G) Staining indexes of IHC assays. Data are represented as mean ± standard error of the mean (*P < 0.05, **P < 0.01).

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