Key features and details
- Rabbit polyclonal to Vinculin
- Suitable for: IHC-P, WB, IP
- Reacts with: Mouse, Human
- Isotype: IgG
Product nameAnti-Vinculin antibody
See all Vinculin primary antibodies
DescriptionRabbit polyclonal to Vinculin
Tested applicationsSuitable for: IHC-P, WB, IPmore details
Species reactivityReacts 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
- HeLa, 293T or NIH3T3 whole cell lysate.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferPreservative: 0.09% Sodium azide
Constituent: Tris citrate/phosphate
Concentration information loading...
PurityImmunogen affinity purified
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.
|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.|
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.
modificationsPhosphorylated; 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
- CMD1W antibody
- CMH15 antibody
- Epididymis luminal protein 114 antibody
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
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human breast carcinoma tissue labelling Vinculin with ab91459 at 1/1000 (1µg/ml). Detection: DAB.
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.
ab91459 has been referenced in 3 publications.
- Hirth S et al. Paxillin and Focal Adhesion Kinase (FAK) Regulate Cardiac Contractility in the Zebrafish Heart. PLoS One 11:e0150323 (2016). WB, IF . PubMed: 26954676
- 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 . PubMed: 24573681
- Thompson WR et al. Mechanically activated Fyn utilizes mTORC2 to regulate RhoA and adipogenesis in mesenchymal stem cells. Stem Cells 31:2528-37 (2013). PubMed: 23836527