PrPSc as a product of membrane folding

Abstract

The features of the course of transmissible spongiform encephalopathies have been correlated with the regularities of protein structure formation and their interaction with cell membranes. Evidence is given about the mechanism of formation of the pathogenic isoform of the prion protein as a consequence of membrane folding of the protein with incomplete structure formation. Thus, the reproduction of the pathogenic form of the prion protein takes on the character of a cellular process, and not an intermolecular process, as is commonly believed.