Polyclonal Antibody to VASP (Phospho-Ser157)
Figure 1: Western blot analysis of extracts from C6 cells untreated or treated with PMA using VASP(Phospho-Ser157) Antibody 35-1200 .
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| Format : | Purified |
| Amount : | 100 µl |
| Isotype : | Rabbit IgG |
| Content : | Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. |
| Storage condition : | Store the antibody at 4°C, stable for 6 months. For long-term storage, store at -20°C. Avoid repeated freeze and thaw cycles. |
Ena/VASP proteins are actin-associated proteins involved in a range of processes dependent on cytoskeleton remodeling and cell polarity such as axon guidance, lamellipodial and filopodial dynamics, platelet activation and cell migration. VASP promotes actin filament elongation. It protects the barbed end of growing actin filaments against capping and increases the rate of actin polymerization in the presence of capping protein. VASP stimulates actin filament elongation by promoting the transfer of profilin-bound actin monomers onto the barbed end of growing actin filaments. Plays a role in actin-based mobility of Listeria monocytogenes in host cells. Regulates actin dynamics in platelets and plays an important role in regulating platelet aggregation.
Predicted MW: 50kd, Western blotting: 1:500~1:1000, Immunohistochemistry: 1:50~1:100
For Research Use Only. Not for use in diagnostic/therapeutics procedures.
| Subcellular location: | Cytoplasm, Cytoplasm, Cell junction, Cell junction, Cell projection, Cell projection |
| Post transnational modification: | Major substrate for cAMP-dependent (PKA) and cGMP-dependent protein kinase (PKG) in platelets. The preferred site for PKA is Ser-157, the preferred site for PKG/PRKG1, Ser-239. In ADP-activated platelets, phosphorylation by PKA or PKG on Ser-157 leads to fibrinogen receptor inhibition. Phosphorylation on Thr-278 requires prior phosphorylation on Ser-157 and Ser-239. In response to phorbol ester (PMA) stimulation, phosphorylated by PKC/PRKCA. In response to thrombin, phosphorylated by both PKC and ROCK1. Phosphorylation at Thr-278 by AMPK does not require prior phosphorylation at Ser-157 or Ser-239. Phosphorylation at Ser-157 by PKA is required for localization to the tight junctions in epithelial cells. Phosphorylation modulates F-actin binding, actin filament elongation and platelet activation. Phosphorylation at Ser-322 by AMPK also alters actin filament binding. Carbon monoxide (CO) promotes phosphorylation at Ser-157, while nitric oxide (NO) promotes phosphorylation at Ser-157, but also at Ser-239. Response to NO and CO is blunted in platelets from diabetic patients, and VASP is not phosphorylated efficiently at Ser-157 and Ser-239. |
| Tissue Specificity: | Highly expressed in platelets. |
| BioGrid: | 113251. 92 interactions. |
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