Wednesday, October 26, 2005, 11:00 am — John Dunn Seminar Room, Bldg. 463
Amyloid fibres are hallmarks of prion diseases such as Alzheimer's, Parkinson's disease and many others. Whereas the protein carriers of these diseases have been in many cases identified, the mechanisms by which normal proteins are transformed into amyloid fibres largely remain undisclosed. We have revealed transformation by which two domain-swapped dimers of a cystatin are transformed into tetramers by a yet unidentified process of extensive intermolecular contacts, termed loop swapping.
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