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Sigma-Aldrich

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

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
Research Sub Category
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 Code

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
Beatrice B Yaroslavskiy et al.
Journal of cell science, 118(Pt 23), 5479-5487 (2005-11-18)
The osteoclast degrades bone in cycles; between cycles, the cell is motile. Resorption occurs by acid transport into an extracellular compartment defined by an alphavbeta3 integrin ring. NO has been implicated in the regulation of bone turnover due to stretch
Insulin stimulates glucose transport via nitric oxide/cyclic GMP pathway in human vascular smooth muscle cells.
Bergandi, L; Silvagno, F; Russo, I; Riganti, C; Anfossi, G; Aldieri, E; Ghigo, D; Trovati et al.
Arteriosclerosis, Thrombosis, and Vascular Biology null

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