Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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DNA / chemistry
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DNA / metabolism
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Nucleic Acids* / chemistry
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Nucleic Acids* / metabolism
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PrPC Proteins* / chemistry
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PrPC Proteins* / metabolism
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PrPSc Proteins / chemistry
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PrPSc Proteins / metabolism
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Protein Conformation*
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Protein Folding
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Recombinant Proteins / chemistry
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Recombinant Proteins / metabolism
Substances
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Nucleic Acids
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PrPC Proteins
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PrPSc Proteins
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Recombinant Proteins
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DNA