HTS016C - ChemiSCREEN™ Human C3aR Anaphylotoxin Receptor Calcium-Optimized Stable Cell Line

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    C3a, along with C4a and C5a, is a 77 amino acid anaphylotoxin generated by proteolytic cleavage during activation of the complement pathway (Ember and Hugli, 1997).  The anaphylotoxins strongly promote inflammation by recruiting leukocytes, particularly basophils, eosinophils, neutrophils and monocyte (Martin et al., 1997).  The proinflammatory properties of C3a are mediated by interaction between the peptide and a 7-TM G-protein coupled receptor, C3aR (Crass et al., 1996).  Genetic and pharmacological inhibition of C3a/C3aR interaction indicates an important role for C3aR in allergic asthma (Humbles et al.,  2000; Drouin et al.,  2002).  C3a/C3aR also enhances the effect of SDF-1 in promoting retention of haematopoietic stem/progenitor cells within the bone marrow (Rataiczak et al., 2004).  The cloned human C3aR-expressing cell line is made in the Chem-1 host, which supports high levels of recombinant C3aR expression on the cell surface and contains high levels of the promiscuous G protein Gα15 to couple the receptor to the calcium signaling pathway.  Thus, the cell line is an ideal tool for screening for antagonists of interactions between C3aR and its ligand C3a. 

    Additional Resource :  HTS016C050515 Datasheet

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    Contents: 2 vials of mycoplasma-free cells, 1 ml per vial.
    Storage: Vials are to be stored in liquid N2.
    Applications: Calcium Flux Assay
    Host Cell: Chem-1, an adherent cell line expressing the promiscuous G-protein, Gα15.
    Exongenous Gene Expression: Human C3aR cDNA (Accession Number: U28488) and promiscuous G protein are expressed in a bicistronic vector
    GMO: This product contains genetically modified organisms.
    Reference 1: 1. Ember, JA and Hugli, TE (1997) Complement factors and their receptors. Immunopharmacology 38: 3-15
    Reference 2: 2. Martin, U, et al. (1997) The human C3a receptor is expressed on neutrophils and monocytes, but not on B or T lymphocytes. J. Exp. Med. 186: 199-207.
    Reference 3: 3. Crass T, et al. (1996) Expression cloning of the human C3a anaphylatoxin receptor (C3aR) from differentiated U-937 cells. Eur. J. Immunol. 26: 1944-50.
    Reference 4: 4. Humbles AA, et al. (2000) A role for the C3a anaphylatoxin receptor in the effector phase of asthma. Nature 406: 998-1001.
    Reference 5: 5. Drouin SM, et al. (2002) Absence of the complement anaphylatoxin C3a receptor suppresses Th2 effector functions in a murine model of pulmonary allergy.J. Immunol. 169: 5926-33.
    Reference 6: 6. Ratajczak J, et al. (2004) Mobilization studies in mice deficient in either C3 or C3a receptor (C3aR) reveal a novel role for complement in retention of hematopoietic stem/progenitor cells in bone marrow. Blood 103: 2071-8.