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Normal development and behavior of mice lacking the neuronal cell-surface prp protein

Academic Article
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  • Additional Document Info
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Overview

authors

  • Bueler, H.
  • Fischer, M.
  • Lang, Y.
  • Bluethmann, H.
  • Lipp, H. P.
  • Dearmond, S. J.
  • Prusiner, S. B.
  • Aguet, M.
  • Weissmann, Charles

publication date

  • April 1992

journal

  • Nature  Journal

abstract

  • PrPC is a host protein anchored to the outer surface of neurons and to a lesser extent of lymphocytes and other cells. The transmissible agent (prion) responsible for scrapie is believed to be a modified form of PrPC. Mice homozygous for disrupted PrP genes have been generated. Surprisingly, they develop and behave normally for at least seven months, and no immunological defects are apparent. It is now feasible to determine whether mice devoid of PrPC can propagate prions and are susceptible to scrapie pathogenesis.

subject areas

  • Aging
  • Animals
  • Base Sequence
  • Blastocyst
  • Blotting, Northern
  • Blotting, Western
  • Brain
  • Cell Membrane
  • Crosses, Genetic
  • Female
  • Genetic Carrier Screening
  • Male
  • Membrane Proteins
  • Mice
  • Molecular Sequence Data
  • Neurons
  • Oligodeoxyribonucleotides
  • Polymerase Chain Reaction
  • PrPSc Proteins
  • Pregnancy
  • Prions
  • RNA
  • Recombination, Genetic
  • Restriction Mapping
  • Scrapie
  • Stem Cells
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Identity

International Standard Serial Number (ISSN)

  • 0028-0836

Digital Object Identifier (DOI)

  • 10.1038/356577a0

PubMed ID

  • 1373228
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Additional Document Info

start page

  • 577

end page

  • 582

volume

  • 356

issue

  • 6370

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