Literature DB >> 17708907

Prion protein and the transmissible spongiform encephalopathies.

B Caughey, B Chesebro.   

Abstract

Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases that occur in a wide variety of mammals. In humans, TSE diseases include kuru, sporadic and iatrogenic Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), and fatal familial insomnia (FFI). So far, TSE diseases occur only rarely in humans; however, scrapie is a widespread problem in sheep, and the recent epidemic of bovine spongiform encephalopathy (BSE or mad cow disease) has seriously affected the British cattle industry. Of special concern is the recent appearance of a new variant of CJD in humans that is suspected of being caused by infections from BSE-infected cattle products. In all these diseases, an abnormal form of a host protein, prion protein (PrP), is essential for the pathogenic process. The relationship of this protein to the transmissible agent is currently the subject of great interest and controversy and is the subject of this review.

Entities:  

Year:  1997        PMID: 17708907     DOI: 10.1016/S0962-8924(96)10054-4

Source DB:  PubMed          Journal:  Trends Cell Biol        ISSN: 0962-8924            Impact factor:   20.808


  53 in total

1.  Population dynamics of scrapie in a sheep flock.

Authors:  M E Woolhouse; L Matthews; P Coen; S M Stringer; J D Foster; N Hunter
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  1999-04-29       Impact factor: 6.237

2.  The basic reproduction number for scrapie.

Authors:  L Matthews; M E Woolhouse; N Hunter
Journal:  Proc Biol Sci       Date:  1999-05-22       Impact factor: 5.349

3.  Species-independent inhibition of abnormal prion protein (PrP) formation by a peptide containing a conserved PrP sequence.

Authors:  J Chabry; S A Priola; K Wehrly; J Nishio; J Hope; B Chesebro
Journal:  J Virol       Date:  1999-08       Impact factor: 5.103

4.  Lysosomotropic agents and cysteine protease inhibitors inhibit scrapie-associated prion protein accumulation.

Authors:  K Doh-Ura; T Iwaki; B Caughey
Journal:  J Virol       Date:  2000-05       Impact factor: 5.103

5.  The signature of scrapie: differences in the PrP genotype profile of scrapie-affected and scrapie-free UK sheep flocks.

Authors:  M Baylis; F Houston; W Goldmann; N Hunter; A R McLean
Journal:  Proc Biol Sci       Date:  2000-10-22       Impact factor: 5.349

6.  Wild-type PrP and a mutant associated with prion disease are subject to retrograde transport and proteasome degradation.

Authors:  J Ma; S Lindquist
Journal:  Proc Natl Acad Sci U S A       Date:  2001-12-11       Impact factor: 11.205

7.  The [KIL-d] element specifically regulates viral gene expression in yeast.

Authors:  Z Tallóczy; R Mazar; D E Georgopoulos; F Ramos; M J Leibowitz
Journal:  Genetics       Date:  2000-06       Impact factor: 4.562

8.  Strain-specified relative conformational stability of the scrapie prion protein.

Authors:  D Peretz; M R Scott; D Groth; R A Williamson; D R Burton; F E Cohen; S B Prusiner
Journal:  Protein Sci       Date:  2001-04       Impact factor: 6.725

9.  The interplay of glycosylation and disulfide formation influences fibrillization in a prion protein fragment.

Authors:  Carlos J Bosques; Barbara Imperiali
Journal:  Proc Natl Acad Sci U S A       Date:  2003-06-12       Impact factor: 11.205

Review 10.  Functional aspects of cellular microcompartmentation in the development of neurodegeneration: mutation induced aberrant protein-protein associations.

Authors:  Judit Ovádi; Ferenc Orosz; Susan Hollán
Journal:  Mol Cell Biochem       Date:  2004 Jan-Feb       Impact factor: 3.396

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