Advances in Human Genetics by John B. Graham, Emily S. Barrow, Howard M. Reisner (auth.),

By John B. Graham, Emily S. Barrow, Howard M. Reisner (auth.), Harry Harris, Kurt Hirschhorn (eds.)

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The researchers believe that the component chains (Mr 166,000, 130,000, and 76,000) are associated through Ca2 + bridges, since EDT A treatment resulted in loss of activity and disappearance of the two larger components. Porcine VIII:C was also specifically bound by an in solubilized antibody to human VIII:C antibody (Knutson and Fass, 1982). 8 buffer was coagulationally inactive, it gave the same SDS-PAGE bands, before and after thrombin treatment, as the active porcine VIII:C obtained by absorption to the monoclonal antibody.

VIII coagulant peptide, while numeral 2 refers to all genes in the pathway controlling production of VIIIR:Ag. The genetic symbol aa + refers to the structural information that codes the peptide, while rr+ refers to genetic information that affects the rate of production ofa peptide in some fashion. Classic hemophilia is viewed as the result of mutation of the structural gene, while dominant hemophilia A probably results from mutation of a regulatory gene. Classic vWd probably results from mutation of a regulatory gene.

V activity. Fifteen individuals not believed to be congenitally deficient in F. V have been reported as having developed spontaneous inhibitors (antibodies) to this clotting factor. Eight of the inhibitors have been characterized as immunoglobulin G (IgG), one as IgM and IgG, and one as IgA and IgG. Six of the 15 patients had been treated previously with streptomycin and seven with penicillin. All but one of the six have been shown to have both K and}.. light chains (Feinstein, 1982). One patient with congenital F.

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