产品: Vimentin 抗体
货号: AF7013
描述: Rabbit polyclonal antibody to Vimentin
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Rabbit, Dog, Chicken, Xenopus
蛋白号: P08670
RRID: AB_2835318

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产品描述

来源:
Rabbit
应用:
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: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
Vimentin Antibody detects endogenous levels of total Vimentin.
RRID:
AB_2835318
引用格式: Affinity Biosciences Cat# AF7013, RRID:AB_2835318.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

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

抗原和靶标

免疫原:

A synthesized peptide derived from human Vimentin

基因/基因ID:
描述:
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.

研究领域

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

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

文献引用

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). 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)

7). 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

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). Engineering of phosphatidylserine-targeting ROS-responsive polymeric prodrug for the repair of ischemia-reperfusion-induced acute kidney injury. Journal of controlled release : official journal of the Controlled Release Society, 2024 (PubMed: 39486459) [IF=10.5]

10). 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.

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