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The post-translational conversion of the ubiquitously expressed cellular form of the prion protein, PrP C , into its misfolded and pathogenic isoform, known as prion or PrP Sc , plays a key role in prion diseases. These maladies are denoted transmissible spongiform encephalopathies (TSEs) and affect both humans and animals. A prerequisite for understanding TSEs is unraveling the molecular mechanism leading to the conversion process whereby most α-helical motifs are replaced by β-sheet secondarydoi:10.3390/molecules18089451 pmid:23966072 fatcat:c45bdswqyzaabel6pf2jwnklsq