Overview

  • Product nameAnti-Vinculin antibody
    See all Vinculin primary antibodies
  • Description
    Rabbit polyclonal to Vinculin
  • Tested applicationsSuitable for: IHC-P, WB, IPmore details
  • Species reactivity
    Reacts with: Mouse, Human
    Predicted to work with: Rat, Rabbit, Horse, Chicken, Guinea pig, Cow, Turkey, Pig, Chimpanzee, Zebrafish, Rhesus monkey, Gorilla, Tilapia, Orangutan, Medaka fish, Platypus (Ornithorhynchus anatinus)
  • Immunogen

    Synthetic peptide corresponding to a region within C terminal amino acids 1016 - 1066 (SEQATEMLVH NAQNLMQSVK ETVREAEAAS IKIRTDAGFT LRWVRKTPWY Q) of Human Vinculin (NP_003364.1).

  • Positive control
    • HeLa, 293T or NIH3T3 whole cell lysate.

Properties

Applications

Our Abpromise guarantee covers the use of ab91459 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P 1/500 - 1/2000. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
WB 1/2000 - 1/10000. Predicted molecular weight: 124 kDa.
IP Use at 5-15 µg/mg of lysate.

Target

  • FunctionActin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.
  • Tissue specificityMetavinculin is muscle-specific.
  • Involvement in diseaseDefects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:611407]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
    Defects in VCL are the cause of cardiomyopathy familial hypertrophic type 15 (CMH15) [MIM:613255]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.
  • Sequence similaritiesBelongs to the vinculin/alpha-catenin family.
  • DomainExists in at least two conformations. When in the closed, 'inactive' conformation, extensive interactions between the head and tail domains prevent detectable binding to most of its ligands. It takes on an 'active' conformation after cooperative and simultaneous binding of two different ligands. This activation involves displacement of the head-tail interactions and leads to a significant accumulation of ternary complexes. The active form then binds a number of proteins that have both signaling and structural roles that are essential for cell adhesion.
    The N-terminal globular head (Vh) comprises of subdomains D1-D4. The C-terminal tail (Vt) binds F-actin and cross-links actin filaments into bundles. An intramolecular interaction between Vh and Vt masks the F-actin-binding domain located in Vt. The binding of talin and alpha-actinin to the D1 subdomain of vinculin induces a helical bundle conversion of this subdomain, leading to the disruption of the intramolecular interaction and the exposure of the cryptic F-actin-binding domain of Vt. Vt inhibits actin filament barbed end elongation without affecting the critical concentration of actin assembly.
  • Post-translational
    modifications
    Phosphorylated; on serines, threonines and tyrosines. Phosphorylation on Tyr-1133 in activated platelets affects head-tail interactions and cell spreading but has no effect on actin binding nor on localization to focal adhesion plaques.
    Aceylated; mainly by myristic acid but also small amount of palmitic acid.
  • Cellular localizationCytoplasm > cytoskeleton. Cell junction > adherens junction. Cell membrane. Cytoplasmic face of adhesion plaques. Recruitment to cell-cell junctions occurs in a myosin II-dependent manner. Interaction with CTNNB1 is necessary for its localization to the cell-cell junctions.
  • Information by UniProt
  • Database links
  • Alternative names
    • CMD1W antibody
    • CMH15 antibody
    • Epididymis luminal protein 114 antibody
    • HEL114 antibody
    • Metavinculin antibody
    • MV antibody
    • MVCL antibody
    • OTTHUMP00000019861 antibody
    • OTTHUMP00000019862 antibody
    • VCL antibody
    • VINC antibody
    • VINC_HUMAN antibody
    • Vinculin antibody
    see all

Anti-Vinculin antibody images

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human breast carcinoma tissue labelling Vinculin with ab91459 at 1/1000 (1µg/ml). Detection: DAB.
  • All lanes : Anti-Vinculin antibody (ab91459) at 0.1 µg/ml

    Lane 1 : HeLa whole cell lysate at 50 µg
    Lane 2 : HeLa whole cell lysate at 15 µg
    Lane 3 : HeLa whole cell lysate at 5 µg
    Lane 4 : 293T whole cell lysate at 50 µg
    Lane 5 : Mouse NIH3T3 whole cell lysate at 50 µg

    Developed using the ECL technique

    Predicted band size : 124 kDa


    Exposure time : 3 minutes
  • SSA1 was immunoprecipitated from 1mg HeLa whole cell lysate using 10µg ab91459.
    20% of the immunoprecipitate was loaded per lane, and probed with ab91459 at 1µg/ml (lane 1) or a control IgG (lane2).
    Detection: chemoluminescence with an exposure time of 10 seconds.

References for Anti-Vinculin antibody (ab91459)

This product has been referenced in:
  • Simon NC & Barbieri JT Bacillus cereus Certhrax ADP-ribosylates vinculin to disrupt focal adhesion complexes and cell adhesion. J Biol Chem 289:10650-9 (2014). WB ; Human . Read more (PubMed: 24573681) »

See 1 Publication for this product

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