The main hypothesis for prion diseases proposes that the cellular protein (PrP(c)) can be altered into a misfolded, beta-sheet-rich isoform (PrP(Sc)). We describe here that host nucleic acid may catalyze the conversion between PrP(c) and PrP(Sc) isoforms, by reducing the protein mobility and by making the protein-protein interactions more likely. We summarize the findings, focusing in the biological relevance of the catalytic action of nucleic acid.
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Cordeiro et al. (2005) studied this question.
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