Monari L, Chen S G, Brown P, Parchi P, Petersen R B, Mikol J, Gray F, Cortelli P, Montagna P, Ghetti B
Division of Neuropathology, Case Western Reserve University, Cleveland, OH 44106.
Proc Natl Acad Sci U S A. 1994 Mar 29;91(7):2839-42. doi: 10.1073/pnas.91.7.2839.
Fatal familial insomnia and a subtype of Creutzfeldt-Jakob disease, two clinically and pathologically distinct diseases, are linked to the same mutation at codon 178 (Asp-178-->Asn) but segregate with different genotypes determined by this mutation and the methionine-valine polymorphism at codon 129 of the prion protein gene. The abnormal isoforms of the prion protein in these two diseases were found to differ both in the relative abundance of glycosylated forms and in the size of the protease-resistant fragments. The size difference was consistent with a different protease cleavage site, suggesting a different conformation of the protease-resistant prion protein present in the two diseases. These differences are likely to be responsible for the type and location of the lesions that characterize these two diseases. Therefore, the combination of the mutation at codon 178 and the polymorphism at codon 129 determines the disease phenotype by producing two altered conformations of the prion protein.
致死性家族性失眠症和克雅氏病的一个亚型,这两种在临床和病理上截然不同的疾病,与密码子178(天冬氨酸-178→天冬酰胺)处的相同突变相关,但根据该突变以及朊病毒蛋白基因密码子129处的甲硫氨酸-缬氨酸多态性,它们以不同的基因型分离。发现这两种疾病中朊病毒蛋白的异常异构体在糖基化形式的相对丰度以及蛋白酶抗性片段的大小方面均存在差异。大小差异与不同的蛋白酶切割位点一致,表明这两种疾病中存在的蛋白酶抗性朊病毒蛋白具有不同的构象。这些差异可能是导致这两种疾病特征性病变的类型和位置的原因。因此,密码子178处的突变与密码子129处的多态性相结合,通过产生两种改变的朊病毒蛋白构象来决定疾病表型。