抗Vimentin抗体 | Anti-Vimentin Antibody

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Immunocytochemistry/Immunofluorescence: Vimentin Antibody [NB300-223] - analysis of HeLa cell culture stained with chicken pAb to vimentin, NB300-223, dilution 1:10,000 in green, and costained with EnCor mouse mAb to actin, dilution 1:500 in red. The blue is DAPI staining of nuclear DNA. The vimentin antibody stains the intermediate filament network while the actin antibody labels the submembranous cytoskeleton, stress fibers, and bundles of actin associated with cell adhesion sites.

Vimentin Antibody [NB300-223] - Analysis of tissue and cell lysates using chicken pAb to Vimentin, NB300-223, dilution 1:5,000 in red. [1] protein standard (red), [2] rat whole brain lysate, [3] HeLa, [4] SH-SY5Y, [5] HEK293, and [6] NIH-3T3 cell lysates. NB300-223 binds to the vimentin protein showing a single band at ~50 kDa. The blot was simultaneously probed with mouse mAb to MAP2C/D, dilution 1:5,000 in green, revealing multiple bands around 280kDa that correspond to full length MAP2A/2B isotypes, and ~70kDa bands which are MAP2C/D isotypes. MAP2 isotypes are seen only in extracts containing neuronal lineage cells.

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Background

Vimentin (VIM) is a widely expressed/highly conserved member of type III intermediate filaments (IF) family proteins found in various non-epithelial cells, especially in mesenchymal cells. It exists as homopolymer assembled from elementary dimers and interacts with HCV core protein, LGSN, SYNM, PLEC, SLC6A4, STK33, LARP6 and RAB8B, and its interaction with LARP6 plays a key role in the stabilization of type I collagen mRNAs, CO1A1/CO1A2. VIM's dynamic structural changes and spatial re-organization in response to extracellular stimuli facilitate coordination of various signal transduction pathways. Filament disassembly during cell division is promoted by VIM phosphorylation at Ser-55 as well as by nestin. VIM is phosphorylated by STK33, CDK5 and PKN1; and PKN1 mediated phosphorylation inhibits filaments formation, whereas, CDK5 executes its phosphorylation at Ser-56 during neutrophil secretion in cytoplasm. VIM expression is predominant during embryonic development, while in adults, its expression is limited to connective tissue mesenchymal cells, CNS and muscles. VIM has emerged as canonical marker of EMT (epithelial to mesenchymal transition- a process that renders the epithelial cells to dramatically alter their shape and acquire increased motility) which is characterized by the expression of VIM IFs in epithelial cells that normally express only keratin IFs and enhanced VIM expression has been reported in various cancers where it plays as a driving factor for metastasis.

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