The coding sequence of the hemolytically inactive C4A6 allotype of human complement component C4 reveals that a single arginine to tryptophan substitution at beta-chain residue 458 is the likely cause of the defect.

M J Anderson, C M Milner, R G Cotton, R D Campbell

    Research output: Contribution to journal › Article › peer-review

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    Immunology and Microbiology