Mouse CD36/SR-B3 Antibody
Mouse CD36/SR-B3 Antibody Summary
Accession # Q08857
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
CD36 (alternatively known as platelet membrane glycoprotein IV (GPIV), thrombospondin receptor, fatty acid translocase (FAT), and scavenger receptor class B, member 3 (SR-B3)) is an 88 kDa, integral membrane glycoprotein that belongs to the class B scavenger receptor family (1, 2). The molecule is described as being ditopic, with two transmembrane segments connected by an extracellular loop (3). Mouse CD36 is synthesized as a 472 amino acid (aa) protein that contains a 6 aa N‑terminal cytoplasmic domain, a 22 aa N‑terminal transmembrane segment, a 420 aa extracellular “loop”, a 22 aa C‑terminal transmembrane segment, and a 9 aa C‑terminal cytoplasmic tail (4). Both cytoplasmic tails are palmitoylated, with the C‑terminal tail involved in oxidized LDL binding (5, 6). With respect to the extracellular loop, the N‑terminal region is believed to bind both thrombospondin-1 and Plasmodium-infected erythrocytes. Other ligands for CD36 include long-chain fatty acids, collagen, phospholipids and apoptotic cells (1). The extracellular loop of mouse CD36 is 94%, 92%, 84%, and 84% aa identical to the extracellular loops of rat, hamster, human, and bovine CD36, respectively. Cells known to express CD36 include capillary endothelium, adipocytes, skeletal muscle cells, intestinal epithelium, smooth muscle cells, and hematopoietic cells such as red blood cells, platelets, and monocytes (1). On the surface of cells, CD36 is suggested to exist as a dimer in response to ligation (7). CD36 is reported to regulate fatty uptake, act as an angiogenic with TSP-1, and participate in the clearance of apoptotic phagocytes (1, 8).
- Febbraio, M. et al. (2001) J. Clin. Invest. 108:795.
- Silverstein, R.L. and M. Febbraio (2000) Curr. Opin. Lipid. 11:483.
- Gruarin, P. et al. (2000) Biochem. Biophys. Res. Commun. 275:446.
- Endemann, G. et al. (1993) J. Biol. Chem. 268:11811.
- Malaud, E. et al. (2002) Biochem. J. 364:507.
- Tao, N. et al. (1996) J. Biol. Chem. 271:22315.
- Daviet, L. et al. (1997) Thromb. Haemost. 78:897.
- Simantov, R. and R.L. Silverstein (2003) Front. Biosci. 8:s874.
Citation for Mouse CD36/SR-B3 Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
1 Citation: Showing 1 - 1
Activation of AMPKalpha2 is not crucial for mitochondrial uncoupling-induced metabolic effects but required to maintain skeletal muscle integrity.
Authors: Ost M, Werner F, Dokas J, Klaus S, Voigt A
PLoS ONE, 2014;9(4):e94689.
Sample Types: Tissue Homogenates
Applications: Western Blot
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