05-611
Anti-phospho-VASP (Ser239) Antibody, clone 16C2
clone 16C2, Upstate®, from mouse
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
16C2, monoclonal
species reactivity
mouse, rat, human
manufacturer/tradename
Upstate®
technique(s)
flow cytometry: suitable
immunocytochemistry: suitable
western blot: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
phosphorylation (pSer239)
Gene Information
human ... VASP(7408)
Related Categories
Specificity
Based on sequence homology this antibody is also predicted to cross-react with dog and cow.
phosphorylated VASP
Immunogen
phospho-peptide corresponding to amino acids 236-242 of human phospho-VASP (RKV[pS]KQE)
Application
Research Category
Signaling
Signaling
Research Sub Category
Cytoskeletal Signaling
Cytoskeletal Signaling
This Anti-phospho-VASP (Ser239) Antibody, clone 16C2 is validated for use in FC, WB, IC for the detection of phospho-VASP (Ser239).
Quality
routinely evaluated by immunoblot on RIPA lysates from CTLL cells
Target description
50kDa
Physical form
100µg of mouse IgG1 from serum-free cell culture supernatant, purified by thiophilic adsorption and size exclusion chromatography. Lyophilized from 1ml of PBS, 0.1% sodium azide, PEG and sucrose. Lyophilized powder. Reconstitute with 100 µL H2O (15 min, RT) for a final concentration of 1 mg/mL. Store at -20°C.
Format: Purified
Thiophilic adsorption chromatography
Storage and Stability
2 years at -20°C
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
10 - Combustible liquids
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Olena Rudyk et al.
Circulation, 126(3), 287-295 (2012-06-12)
Although nitroglycerin has remained in clinical use since 1879, the mechanism by which it relaxes blood vessels to lower blood pressure remains incompletely understood. Nitroglycerin undergoes metabolism that generates several reaction products, including oxidants, and this bioactivation process is essential
Jonel Trebicka et al.
Hepatology (Baltimore, Md.), 47(4), 1264-1276 (2008-03-06)
In cirrhosis, splanchnic vasodilation contributes to portal hypertension, subsequent renal sodium retention, and formation of ascites. Urotensin II(U-II) is a constrictor of large conductive vessels. Conversely, it relaxes mesenteric vessels, decreases glomerular filtration, and increases renal sodium retention. In patients
Susan L Lindsay et al.
Journal of cell science, 120(Pt 17), 3011-3021 (2007-08-09)
The initial step in directed cell movement is lamellipodial protrusion, an action driven by actin polymerization. Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) family proteins are key regulators of this actin polymerization and can control lamellipodial protrusion rate. Ena/VASP proteins are substrates for modification
I Kishimoto et al.
Journal of neuroendocrinology, 20(11), 1213-1223 (2008-08-30)
Cyclic GMP (cGMP) is known to play important roles for neuronal development and neurite pathfinding. However, the regulatory mechanism that governs the synthesis of cGMP in the nervous system is not well defined. In the present study, we examined the
A Mülsch et al.
Circulation, 103(17), 2188-2194 (2001-05-23)
Chronic in vivo treatment with nitroglycerin (NTG) induces tolerance to nitrates and cross-tolerance to nitrovasodilators and endothelium-derived nitric oxide (NO). We previously identified increased vascular superoxide formation and reduced NO bioavailability as one causal mechanism. It is still controversial whether
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