Browse our anti-Vimentin (VIM) Antibodies

Human Vimentin (VIM) interaction partners

1. These data show that vimentin is required for lung adenocarcinoma metastasis by maintaining heterotypic tumor cell-CAF interactions during collective invasion.

2. this study shows that methylation status of VIM gene changes in breast cancer

3. vimentin may play an important role in the progression of glioblastoma multiforme

4. overexpression of the epithelial to mesenchymal transition marker vimentin is associated with poor clinical outcome in older patients with cytogenetically normal acute myeloid leukemia.

5. Assembly Kinetics of Vimentin Tetramers

6. The crystal structure of coil 1B of human vimentin reveals how coiled coil dimers may assemble into a high-order filamentous structure.

7. Therefore, the present study demonstrated that ZEB1 is a potential biomarker of the tumorigenesis and progression of HCC, and it may regulate transcription of the VIM gene.

8. vimentin and nestin intermediate filaments interact with caveolae central component caveolin-1 (CAV-1) and importantly, restrain the intracellular trafficking of CAV-1 positive vesicles by serving as a physical barrier.

9. Cell analyses revealed that all major cytoskeleton components were disrupted during pyroptosis and that sensitivity to rupture was calpain-dependent and linked with cleavage of vimentin and loss of intermediate filaments.

10. extracellular vimentin may play an important role in cancer or trauma-complications by inducing suppression of the adaptive immune response. In a positive sense, the presence of extracellular vimentin may prevent tissue-damage from contributing to the development of autoimmunity.

11. VIM is downregulated and E-cad is upregulated in T1 stage non-small-cell lung cancer, suggesting that a mesenchymal-epithelial transition may take place in the early-stage of tumor development

12. aberrant methylation of SOX1 and VIM promoters may be potential biomarkers for noninvasive detection of hepatocellular carcinoma and metastasis

13. cell surface vimentin was identified as a candidate surface receptor mediating stiffness-dependent adhesion of Listeria monocytogenes to human microvascular endothelial cells.

14. shape and inner structure of these mutant filaments is significantly altered

15. Vimentin and Sam68, are identified as bona fide SRMS substrates through in vitro and in vivo assays.

16. Review includes a brief historical account of early studies that unveiled vimentin as a unique component of the cell cytoskeleton followed by an overview of the physiological vimentin functions

17. Involved in clear cell renal carcinoma vasculogenic mimicry and metastasis through association with TR4 nuclear receptor and miR490-3p

18. Study reported for the first time that one of the proteins that binds to P5 in U251 glioblastoma cells is vimentin, and the present findings indicated that P5 may be an attractive target for novel molecular targeted therapy of glioblastoma.

19. Mechanistic analyses revealed that FOXD1 expressed its oncogenic characteristics through activating Vimentin in non-small cell lung cancer cells.

20. Results showed that BPIFB1 expression markedly inhibited NPC cell migration, invasion, and lung-metastatic abilities. Additionally, identification of two BPIFB1-interacting proteins, VTN and VIM, showed that BPIFB1 reduced VTN expression and the formation of a VTN-integrin alphaV complex in NPC cells, leading to inhibition of the FAK/Src/ERK signalling pathway.

Mouse (Murine) Vimentin (VIM) interaction partners

1. the results show the implication of FAs both in ECs and vascular SMCs in the role of vimentin in arterial stiffening.

2. mutation of the serine sites phosphorylated in vimentin during mitosis alters intermediate filament protein expression but has no effect on astrocyte morphology or proliferation, and leads to increased neuronal differentiation of neural progenitor cells.

3. The Listeria monocytogenes virulence factor InlF was found to bind vimentin and was necessary for optimal bacterial colonization of the brain.

4. MAGE-G1 interacted with fascin 1 or vimentin in P19 cells after a 6-day retinoic acid-induced neuronal differentiation.

5. Results found that the absence of vimentin impairs spontaneous endothelial differentiation in vitro and have furthering the understanding of the regulators of differentiation.

6. Results indicate that vimentin orchestrates the healing by controlling fibroblast proliferation, TGF-beta1-Slug signaling, and epithelial-mesenchymal transition (EMT) processing, and all of which in turn govern the required keratinocyte activation.

7. Protein phosphatase 1 is a key protein serine/threonine phosphatase that controls vimentin Ser-56 dephosphorylation in smooth muscle.

8. These findings identify vimentin as a positive regulator of stemness in the developing mouse mammary gland and in breast cancer cells.

9. This study is the first to show that vimentin has an important role in tumor metastasis in vivo in the setting of pre-diabetes and endogenous hyperinsulinemia.

10. These findings identify two specific sites on vimentin that are phosphorylated by Cadmium.

11. The expression level of vimentinin liver cirrhotic tissues were significantly higher than that in chronic hepatitis tissues.

12. both arthritis-susceptible and -resistant mice can generate cellular and humoral immunity to Vim.

13. vimentin knockout neurons were insensitive to the axonotrophic effects of Clostridium botulinum C3 exoenzyme

14. These findings suggest that Plk1 regulates smooth muscle contraction by modulating vimentin phosphorylation at Ser-56.

15. findings thus show that the inability to produce GFAP and Vim affects normal retinal physiology and that the effect of IF deficiency on retinal cell survival differs, depending on the underlying pathologic condition

16. these findings identify a hereto-unappreciated role for serine-38 phosphorylated vimentin as an important determinant of myofibroblast sensitivity to Withaferin A.

17. Vimentin expression increased after traumatic brain injury and was positively correlated with edema and neurological impairments.

18. Annexin, lamin, and vimentin were identified as universal dystrophic markers

19. Astrocytes deficient of GFAP and vimentin showed decreased Notch signal sending competence and altered expression of Notch signaling pathway-related genes

20. Absence of GFAP, or both GFAP and vimentin, alters Alzheimer's disease-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a higher inflammatory expression profile

Zebrafish Vimentin (VIM) interaction partners

1. Taken together these findings suggest that reactive oxygen species and vimentin integrate early wound signals to orchestrate the formation of collagen-based projections that guide regenerative growth during efficient wound repair.

2. Knockdown of filamin A or vimentin in normal cells profoundly suppresses apical extrusion of the neighbouring transformed cells.

Cow (Bovine) Vimentin (VIM) interaction partners

1. Immunocytochemistry for Vimentin detection in nuclei of IVF and NT bovine embryos

2. These results indicate that the inner mass differentiates dynamically in blastocysts, as reflected by the expression of vimentin; higher vimentin expression may reflect the higher developmental competence of embryos.

3. an intact vimentin intermediate filament network contributes to the maintenance of the chondrocyte phenotype

Atlantic Salmon (Salmo salar) Vimentin (VIM) interaction partners

1. Vimentin- like transcript was expressed in both chordocytes and chordoblasts, whereas the elastin- like transcript was uniquely expressed in the chordoblasts lining the notochordal sheath.

Horse (Equine) Vimentin (VIM) interaction partners

1. This study evaluated the expression pattern of vimentin in testes of mature Arabian stallions and correlated its distribution with grade of seminiferous tubule impairment as indicated by a Johnsen score.

Pig (Porcine) Vimentin (VIM) interaction partners

1. ANXA2 can interact with vimentin and enhance porcine reproductive and respiratory syndrome virus (PRRSV) growth. This contributes to the regulation of PRRSV replication in infected cells and may have implications for the future antiviral strategies.

2. As the inner cell mass forms the epiblast, SSEA1 is lost and VIMENTIN is lost and re-expressed.

3. These observations indicate that vimentin serves as a putative receptor for Japanese encephalitis virus in porcine kidney cells.

4. Interaction of nucleocapsid protein of transmissible gastroenteritis virus with host vimentin is required for virus infection.

5. protein(s) that associated with RPTPbeta in response to IGF-I and IGFBP-2 in vascular smooth muscle cells

6. This study demonstrates that maternal VIM, as a genomic protector, is crucial for nuclear reprogramming in porcine cloned embryos.

Rabbit Vimentin (VIM) interaction partners

1. Vim expression in corneal epithelium is found in a cell population composed of highly motile cells.

2. these findings identify a hereto-unappreciated role for serine-38 phosphorylated vimentin as an important determinant of myofibroblast sensitivity to Withaferin A.

3. These differentially expressed proteins associated with key mechanisms involved in atherosclerosis and signaling mechanisms related with vitamin E.