Key features and details
- Rabbit polyclonal to Vinculin (phospho Y100)
- Suitable for: WB
- Reacts with: Chicken
- Isotype: IgG
Product nameAnti-Vinculin (phospho Y100) antibody
See all Vinculin primary antibodies
DescriptionRabbit polyclonal to Vinculin (phospho Y100)
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Chicken
Predicted to work with: Mouse
Synthetic peptide corresponding to Human Vinculin (phospho Y100). derived from a region that contains tyrosine 100.
Database link: P18206
- COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were treated with vanadate for 24 hr.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: 0.1% BSA, 99% PBS
Concentration information loading...
PurityImmunogen affinity purified
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab200812 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/1000. Predicted molecular weight: 124 kDa.
1/1000. Predicted molecular weight: 124 kDa.
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
Lanes 1-5 : Anti-Vinculin (phospho Y100) antibody (ab200812) at 1/1000 dilution
Lanes 6-10 : Anti-Vinculin pan antibody
Lane 1 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA untreated
Lanes 2 & 7-10 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were treated with vanadate for 24 hr
Lane 3 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were treated with vanadate for 24 hr. with non-phosphopeptide corresponding to the immunogen
Lane 4 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were treated with vanadate for 24 hr with generic phosphotyrosine-containing peptide
Lane 5 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were treated with vanadate for 24 hr with phosphopeptide immunogen
Lane 6 : COS cells co-transfected with activated Src and His-tagged chicken Vinculin cDNA were untreated
Developed using the ECL technique.
Predicted band size: 124 kDa
Following immunoprecipitation of Vinculin with an anti-His monoclonal antibody, proteins were resolved by SDS-PAGE on an 8% polyacrylamide gel and transferred to PVDF.
ab200812 has not yet been referenced specifically in any publications.