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HTS017M - ChemiSCREEN™ C5aR Anaphylotoxin ReceptorMembrane Preparation

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$646.90
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HTS017M
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5 unit(s)
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    C5a is a proinflammatory peptide generated through activation of the complement system, and is more potent than the other anaphylatoxins, C4a and C3a, in activating peripheral blood leukocytes (Gerard and Gerard, 1994). It can actively participate in the regulation of local cytokine network by stimulating production of proinflammatory cytokines (Buchner et al., 1995; Hsu et al., 1999). The proinflammatory effects of C5a are mediated through binding to a specific 7-TM chemoattractant receptor, C5aR (CD88). Binding of C5a to phagocyte C5aR induces chemotaxis, production of superoxide anions, and release of degradative enzymes. Pharmacologic or genetic disruption of C5a/C5aR interaction reduces sepsis (Riedemann et al, 2003), immune complex-induced lung disease (Shushakova et al, 2002), and Arthrogen-induced arthritis (Grant et al, 2002) in experimental models. Cloned human C5a receptor membrane preparations are ideal tools for screening for antagonists of C5a/C5aR interactions.

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    Item Unit of Measure: EA
    Quantity: 200 units
    Storage: On receipt of material store at -70°C. Unopened reagent is stable for a minimum of 1 year from date of shipment when stored at recommended storage temperature. Avoid repeat freeze/thaw cycles. For maximum recovery of product, centrifuge original vial
    Applications: Radioligand Binding Assay
    Host Cell: Chem-1.
    Reference 1: 1. Buchner RR et al. (1995) Expression of functional receptors for human C5a anaphylatoxin (CD88) on the human hepatocellular carcinoma cell line HepG2. Stimulation of acute-phase protein-specific mRNA and protein synthesis by human C5a anaphylatoxin
    Reference 2: 2. Gerard C and Gerard NP (1994) C5A anaphylatoxin and its seven transmembrane-segment receptor. Annu.Rev.Immunol. 12: 775-808.
    Reference 3: 3. Grant EP et al. (2002) Essential role for the C5a receptor in regulating the effector phase of synovial infiltration and joint destruction in experimental arthritis. J. Exp. Med. 196: 1461-1471.
    Reference 4: 4. Hsu MH et al. (1999) NF-kappaB activation is required for C5a-induced interleukin-8 gene expression in mononuclear cells. Blood 93: 3241-3249.
    Reference 5: 5. Riedemann NC et al. (2003) A key role of C5a/C5aR activation for the development of sepsis. J. Leukoc. Biol. 74: 966-970.
    Reference 6: 6. Shushakova N et al. (2002) C5a anaphylatoxin is a major regulator of activating versus inhibitory FcgammaRs in immune complex-induced lung disease. J. Clin. Invest. 110: 1823-30.
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