Homework 2

Electronic Journal / Virtual Library


  1. The 1997 Nobel Prize in Physiology or Medicine is awarded to the American Stanley Prusiner for his pioneering discovery of Prions - a new biological principle of infection. Stanley Prusiner has added prions to the list of well known infectious agents including bacteria , viruses, fungi and parasites. Please find his recently published paper concerning prion diseases and the BSE crisis. Please show the abstract on your homepage and tell me what is BSE.

    BSE is bovine spongiform encephalopathy.

    Abstract:
    Bovine spongiform encephalopathy (BSE) and human Creutzfeldt-Jakob disease (CJD) are among the most notable central nervous system degenerative disorders caused by prions. CJD may present as a sporadic, genetic, or infectious illness. Prions are transmissible particles that are devoid of nucleic acid and seem to be composed exclusively of a modified protein (PrPSc). The normal, cellular prion protein (PrPC) is converted into PrPSc through a posttranslational process during which it acquires a high beta-sheet content. It is thought that BSE is a result of cannibalism in which faulty industrial practices produced prion-contaminated feed for cattle. There is now considerable concern that bovine prions may have been passed to humans, resulting in a new form of CJD.

  2. How many papers is referecned in MEDLINE, on line biomedical abstract service, about prion? How many is concerning its structure? Can you find the paper describe the structure of mouse prion? Please show its abstract on your homepage.

    1306 papers about prion in Medline.
    167 papers decribe prion structure.
    28 papers decribe mouce prion structure.

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

    R Riek, S Hornemann, G Wider, M Billeter, R Glockshuber & K Wuethrich
    Proc Natl Acad Sci U S ANature 382, 180-182 (1996)

    Abstract:
    Spongiform encephalopathies such as scrapie, bovine spongiform encephalopathy and Creutzfeldt-Jakob disease are thought to be caused by a modified pathological form of a 'prion protein' present in normal individuals. Point mutations in certain parts of the prion protein may accelerate the conversion process. Riek et al. have taken a close look at the domain in question. Their study of the mouse prion protein using nuclear magnetic resonance (NMR) spectroscopy shows that this domain contains beta-sheet in addition to the expected alpha-helix. Disease-causing mutations lie within the regions of regular structure or directly adjacent to them, suggesting how the transition to the disease-causing form of the protein might occur.

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