C5AR1/C5R1/CD88 Protein

C5AR1/C5R1/CD88 Protein Overview

C5AR1/C5R1/CD88 reagents

Bao et al. (1992) stated that C5R1, like the receptors for formyl peptides (see 136537) and interleukin-8 (146929), is structurally related to rhodopsin (RHO; 180380) and transduces signals through intracellular GTP-binding proteins. Using microarray analysis of pulmonary gene expression and single nucleotide polymorphism (SNP)-based genotyping, Karp et al. (2000) identified C5 (120900) on mouse chromosome 2 as a susceptibility locus for allergen-induced airway hyperresponsiveness in a mouse model of asthma (see 600807). Backcross and SNP analysis showed that a 2-bp deletion in the C5 gene of A/J and AKR/J mice led to C5 deficiency, correlating with airway hyperresponsiveness, whereas C5-sufficient strains did not develop asthma. Previous studies had shown that administration of IL12 (161560) to susceptible mice renders them resistant to asthma induction (Gavett et al., 1995). Blockade of C5R1 in human monocytes caused marked, dose-dependent inhibition of IL12 production, as well as inhibition of TNFA (191160) secretion and IFNG (147570)-mediated suppression of IL10 (124092) production, although there was no overall effect on IL10 production. These results suggested that C5 deficiency leads to an antiinflammatory phenotype. Karp et al. (2000) noted that previous genomewide screens had found evidence of linkage of asthma susceptibility to the C5 (Ober et al., 1998; Wjst et al., 1999) and C5R1 (Collaborative Study on the Genetics of Asthma, 1997; Ober et al., 1998) chromosomal regions. Antiphospholipid syndrome (107320) is defined by recurrent pregnancy loss and thrombosis in the presence of antiphospholipid antibodies. Therapy for pregnant women with antiphospholipid syndrome is focused on preventing thrombosis, but anticoagulation is only partially successful in averting miscarriage. Girardi et al. (2003) hypothesized that complement activation is a central mechanism of pregnancy loss in antiphospholipid syndrome and tested this in a model in which pregnant mice received human IgG containing antiphospholipid antibodies. They identified complement component C5 (and particularly its cleavage product C5a) and neutrophils as key mediators of fetal injury, and they showed that antibodies or peptides that block C5a-C5a receptor interactions prevent pregnancy complications. This and other findings identified the key innate immune effectors engaged by pathogenic autoantibodies that mediate poor pregnancy outcomes in antiphospholipid syndrome and provided targets for prevention of pregnancy loss in this disorder. Atkinson (2003) commented that since interaction of complement component 5a with its receptor is necessary for thrombosis of placental vasculature, inhibition of complement activation may have a therapeutic role in antiphospholipid syndrome.

C5AR1/C5R1/CD88 protein family

Belongs to the G-protein coupled receptor 1 family.

C5AR1/C5R1/CD88 protein name

Recommended name
C5a anaphylatoxin chemotactic receptor 1
Aliases
C5A, C5AR, CD88

C5AR1/C5R1/CD88 Protein Molecular Weight & PI

The parameters have been computed for the following feature

FT CHAIN 1-350 C5a anaphylatoxin chemotactic receptor 1.

Molecular weight (Da)

39335.56

Theoretical pI

9.22

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