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Prions at the crossroads: the need to identify the active TSE agent
Author(s) -
Nandi P.K.
Publication year - 2004
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.20054
Subject(s) - nucleic acid , endogeny , inducer , in vitro , in vivo , rna , pathogenesis , biology , microbiology and biotechnology , small molecule , prion protein , chemistry , virology , biochemistry , genetics , immunology , gene , medicine , disease , pathology
Structural change in the cellular prion protein, PrP C to a ProteinaseK‐resistant β‐sheet‐rich insoluble form PrP SC and its accumulation have been considered to be central to the pathogenesis of the prion diseases (TSE). In a recent paper, Deleault et al have shown that specific endogenous RNA molecules can induce in vitro structural conversion of endogenous PrP C to PrP SC .1 Small highly structured synthetic RNAs can also induce this conversion process.2 However, recent in vivo results show that PrP SC is not directly involved in the prion pathogenesis.3 It is possible, however, that nucleic‐acid‐induced PrP SC associated with the inducer nucleic acid could be the components of the infectious agent. BioEssays 26:469–473, 2004. © 2004 Wiley Periodicals, Inc.