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Beschreibung

Platelet glycoprotein 4 (UniProt: Q08857, also known as Glycoprotein IIIb, GPIIIB, PAS IV, PAS-4, Platelet glycoprotein IV, GPIV, SR-B2 CD36) is encoded by the cd36 gene (Gene ID: 12491) in murine species. CD36 us a multi-pass membrane glycoprotein with two cytoplasmic domains (aa 1-7 and 462-472), two transmembrane domains (aa 8-29 and 440-461), and one extracellular domain (aa 30-439). It is highly expressed in intestine on the luminal surface of enterocytes. Its expression is also observed in the apical side of lingual taste bunds of circumvallate papillae. Its expression is also reported on monocyte-derived inflammatory macrophages that infiltrate into alveolar spaces, but on alveolar resident macrophages. It serves as a multifunctional protein and acts as a receptor for a broad range of ligands, such as thrombospondin, fibronectin, collagen, oxidized low-density lipoprotein, and bacterial diacylated lipopeptides. It is generally multivalent and can engage multiple receptors simultaneously, resulting in the formation of CD36 clusters that initiate signal transduction and internalization of receptor-ligand complexes. Cellular responses to its ligands are reported to be involved in angiogenesis, inflammatory response, fatty acid metabolism, and dietary fat processing in the intestine. CD36 is shown to bind long-chain fatty acids and facilitate their transport into cells, thereby promoting muscle lipid utilization, gut fat absorption, and adipose energy storage. It is also an important factor in both ventromedial hypothalamus neuronal sensing of long-chain fatty acid and the regulation of energy and glucose homeostasis. CD36 also reported to be a sensor for lipoteichoic acid, a Gram-positive cell wall component, and transmits inflammatory signals in conjunction with TLR2/TLR6 heterodimer and this cluster triggers signaling leading to NF-kB-dependent production of TNF-a via MYD88 signaling pathway. Clone ZND36-6 is an anti-SR-B2 (CD36) blocking antibody that has been used in pulmonary inflammation induced by exposure to silica. (Ref.: Tsugita, M., et al. (2017). Cell Rep. 18(5), 1298-1311, Stewart, CR., et al, (2010). Nat. Immunol. 11(2):155-161, Endemann, G., et al (1993). J. Biol. Chem. 268(16):11811-11816).

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