Literature DB >> 8700211

NMR structure of the mouse prion protein domain PrP(121-231).

R Riek1, S Hornemann, G Wider, M Billeter, R Glockshuber, K Wüthrich.   

Abstract

The 'protein only' hypothesis states that a modified form of normal prion protein triggers infectious neurodegenerative diseases, such as bovine spongiform encephalopathy (BSE), or Creutzfeldt-Jakob disease (CJD) in humans. Prion proteins are thought to exist in two different conformations: the 'benign' PrPcform, and the infectious 'scrapie form', PrPsc. Knowledge of the three-dimensional structure of PrPc is essential for understanding the transition to PrPsc. The nuclear magnetic resonance (NMR) structure of the autonomously folding PrP domain comprising residues 121-231 (ref. 6) contains a two-stranded antiparallel beta-sheet and three alpha-helices. This domain contains most of the point-mutation sites that have been linked, in human PrP, to the occurrence of familial prion diseases. The NMR structure shows that these mutations occur within, or directly adjacent to, regular secondary structures. The presence of a beta-sheet in PrP(121-231) is in contrast with model predictions of an all-helical structure of PrPc (ref. 8), and may be important for the initiation of the transition from PrPc to PrPsc.

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Year:  1996        PMID: 8700211     DOI: 10.1038/382180a0

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  345 in total

1.  Specific binding of normal prion protein to the scrapie form via a localized domain initiates its conversion to the protease-resistant state.

Authors:  M Horiuchi; B Caughey
Journal:  EMBO J       Date:  1999-06-15       Impact factor: 11.598

2.  Molecular modelling indicates that the pathological conformations of prion proteins might be beta-helical.

Authors:  D T Downing; N D Lazo
Journal:  Biochem J       Date:  1999-10-15       Impact factor: 3.857

3.  Sulfated glycans and elevated temperature stimulate PrP(Sc)-dependent cell-free formation of protease-resistant prion protein.

Authors:  C Wong; L W Xiong; M Horiuchi; L Raymond; K Wehrly; B Chesebro; B Caughey
Journal:  EMBO J       Date:  2001-02-01       Impact factor: 11.598

4.  Immobilized prion protein undergoes spontaneous rearrangement to a conformation having features in common with the infectious form.

Authors:  E Leclerc; D Peretz; H Ball; H Sakurai; G Legname; A Serban; S B Prusiner; D R Burton; R A Williamson
Journal:  EMBO J       Date:  2001-04-02       Impact factor: 11.598

5.  Dominant-negative inhibition of prion formation diminished by deletion mutagenesis of the prion protein.

Authors:  L Zulianello; K Kaneko; M Scott; S Erpel; D Han; F E Cohen; S B Prusiner
Journal:  J Virol       Date:  2000-05       Impact factor: 5.103

6.  Cryo-electron microscopy structure of an SH3 amyloid fibril and model of the molecular packing.

Authors:  J L Jiménez; J I Guijarro; E Orlova; J Zurdo; C M Dobson; M Sunde; H R Saibil
Journal:  EMBO J       Date:  1999-02-15       Impact factor: 11.598

7.  Conformational behavior of ionic self-complementary peptides.

Authors:  M Altman; P Lee; A Rich; S Zhang
Journal:  Protein Sci       Date:  2000-06       Impact factor: 6.725

Review 8.  The molecular pathology of CJD: old and new variants.

Authors:  G S Jackson; J Collinge
Journal:  Mol Pathol       Date:  2001-12

9.  Structural studies of the scrapie prion protein by electron crystallography.

Authors:  Holger Wille; Melissa D Michelitsch; Vincent Guenebaut; Surachai Supattapone; Ana Serban; Fred E Cohen; David A Agard; Stanley B Prusiner
Journal:  Proc Natl Acad Sci U S A       Date:  2002-03-12       Impact factor: 11.205

10.  Computational studies on prion proteins: effect of Ala(117)-->Val mutation.

Authors:  Noriaki Okimoto; Kazunori Yamanaka; Atsushi Suenaga; Masayuki Hata; Tyuji Hoshino
Journal:  Biophys J       Date:  2002-05       Impact factor: 4.033

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