Mouse-hamster chimeric prion protein (PrP) devoid of N-terminal residues 23-88 restores susceptibility to 22L prions, but not to RML prions in PrP-knockout mice.

Prion infection induces conformational conversion of the normal prion protein PrPC, into the pathogenic isoform PrPSc, in prion diseases. It has been shown that PrP-knockout (Prnp0/0) mice transgenically reconstituted with a mouse-hamster chimeric PrP lacking N-terminal residues 23-88, or Tg(MHM2Δ23...

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Bibliographic Details
Main Authors: Keiji Uchiyama, Hironori Miyata, Masashi Yano, Yoshitaka Yamaguchi, Morikazu Imamura, Naomi Muramatsu, Nandita Rani Das, Junji Chida, Hideyuki Hara, Suehiro Sakaguchi
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4199594?pdf=render