When Recombinant Human Vitronectin (Catalog # 2308-VN) is immobilized at 2 μg/mL (100 μL/well), Recombinant Cynomolgus Monkey Integrin alpha V beta 3 (Catalog # 10426-AV) binds with an ED50 of 0.04‑0.32 ...read more
2 μg/lane of Recombinant Cynomolgus Monkey Integrin alpha V beta 3 Protein (Catalog # 10426-AV) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue ...read more
Recombinant Cynomolgus Integrin alpha V beta 3 Protein, CF Summary
Details of Functionality
Measured by its binding ability in a functional ELISA.
When Recombinant Human Vitronectin
(Catalog #
2308-VN)
is immobilized at 2 µg/mL (100 µL/well), Recombinant Cynomolgus Monkey Integrin
alpha V beta 3 (Catalog # 10426-AV) binds with an ED50 of 0.06-0.72 μg/mL.
Source
Chinese Hamster Ovary cell line, CHO-derived cynomolgus monkey Integrin alpha V beta 3 protein
Cynomolgus Monkey Integrin alpha V (Phe31-Val992) Accession # XP_005573729.1
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
115 kDa (Integrin alpha V) & 86 kDa (Integrin beta 3). Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
105-160 kDa, under reducing conditions
Publications
Read Publication using 10426-AV in the following applications:
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
6 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after opening.
3 months, -20 to -70 °C under sterile conditions after opening.
Buffer
Supplied as a 0.2 μm filtered solution in PBS with Trehalose.
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Cynomolgus Integrin alpha V beta 3 Protein, CF
antigen identified by monoclonal L230
CD51 antigen
CD51
Integrin alpha V beta 3
integrin alpha-V
integrin, alpha V (vitronectin receptor, alpha polypeptide, antigen CD51)
MSK8
Vitronectin receptor subunit alpha
VNRADKFZp686A08142
Background
Integrin alpha V beta 3 together with alpha IIb beta 3, constitutes the only known beta 3
Integrins (13). The noncovalent heterodimer of 170 kDa alpha V/CD51 and 93 kDa
beta 3/CD61 subunits shows wide expression, notably by endothelial cells and
osteoclasts (24). Each subunit has a transmembrane sequence and a short
cytoplasmic tail connected to the cytoskeleton. Active cell surface alpha V beta 3
adheres to matrix proteins including vitronectin, fibronectin, fibrinogen and
thrombospondin (2, 3). The ligand binding site of
alpha V beta 3 is in the Nterminal head region, formed by interaction of the beta 3
vWFA domain with the alpha V betapropeller structure (4). The alpha V subunit
contributes a "thigh and a calf" region, while the beta 3 subunit contains a PSI
domain and four cysteinerich IEGF folds. The alpha V subunit domains termed thigh,
calf1 and calf2 generate a "knee" region that is bent when the alpha V beta 3 is in its
constitutively inactive state. Activation, either by "inside out" signaling or
by Mg2+ or Mn2+ binding, extends the Integrin to
expose its ligand binding site (1, 4). Within the extracellular domain
(ECD), cynomolgus alpha V shares 99% amino acid (aa) sequence identity with the 962 aa human alpha V,
while cynomolgus beta 3 ECD shares almost 100% aa sequence identity with the 692 aa
human beta 3 ECD. Two splice variants of beta 3 (b and c) diverge over the last 21 amino acids (aa) and lack cytoplasmic phosphorylation sites (5, 6). Another beta 3
splice variant diverges after the vWFA domain, producing a soluble 60 kDa form
in platelets and endothelial cells (7). alpha V beta 3 is essential for the maturation of
osteoclasts and their binding and resorption of bone, as well as promotes their
apoptosis (8, 9). MCSF R and alpha V beta 3 share signaling pathways during
osteoclastogenesis, and deletion of either molecule causes osteopetrosis (8, 9). Cell entry of several viruses is
mediated by alpha V beta 3 (4, 10). alpha V beta 3 is involved in several other signaling pathways
by direct interaction with receptor tyrosine kinases and ligands. For example,
it cooperates with endothelial cell VEGF R2 in
angiogenesis, and with IGF1 to promote cancer
cell proliferation and invasiveness (11, 12).
Hynes, R. O. (2002) Cell 110:673.
Serini, G. et al. (2006) Exp. Cell Res. 312:651.
Ross, F. P. and S. L. Teitelbaum (2005) Immunol. Rev. 208:88.
Xiong, J. et al. (2001) Science 294:339.
Kumar, C. S. et al. (1987) J. Biol. Chem. 272:16390.
vanKuppevelt, H. et al. (1989) Proc. Natl. Acad. Sci. USA 86:5415.
Djaffar, I. et al. (1994) Biochem. J. 300:69.
McHugh, K. P. et al. (2000) J. Clin. Invest. 105:433.
Faccio, R. et al. (2003) J. Clin. Invest. 111:749.
Chu, J. J. and M. Ng (2004) J. Biol. Chem. 279:54533.
Somanath, P.R. et al. (2009) Angiogenesis 12:177.
Saegusa, J. et al. (2009) J. Biol. Chem. 284:24106.
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