Quantitative variations of the C3b/C4b receptor (CR1) in human erythrocytes are controlled by genes within the regulator of complement activation (RCA) gene cluster.
The genetic relationships of quantitative and structural variations of the C3b/C4b receptor (CR1) in human erythrocytes have been analyzed in informative families. Our results demonstrate the existence of multiple discrete quantitative variations of CR1 controlled by a locus, C3bRQ, closely linked to the CR1 structural locus, C3bR. Since the amounts of CR1 produced by each C3bR allele are shown to be independently regulated, we propose that a cis-acting genetic mechanism controls the level of expression of the C3bR alleles, and that this quantitative control plays a major, if not the sole, role in determining the total amounts of CR1 on normal human erythrocytes.
D000483:Alleles; D003167:Complement Activation; D004912:Erythrocytes / Q000032:analysis*; D005809:Genes, Regulator; D006579:Heterozygote; D006801:Humans; D011951:Receptors, Complement / Q000032:analysis / Q000235:genetics*; D017463:Receptors, Complement 3b
D011951:Receptors, Complement; D017463:Receptors, Complement 3b