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SUMMARY:Protein folding homeostasis and prion-like propagation of protein 
 aggregation in neurodegenerative disease - Ron Kopito\, Stanford Universit
 y\, CA USA
DTSTART:20101210T141500Z
DTEND:20101210T160000Z
UID:TALK28217@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:Sequence-specific nucleated protein aggregation underlies the 
 pathogenesis of most neurodegenerative diseases and constitutes the molecu
 lar basis of prion formation.  Nevertheless\, prion disorders have been di
 stinguished from classical neurodegenerative diseases by virtue of their a
 bility to be transmitted between individuals.  In this lecture I will argu
 e that prion-like propagation of pathogenic aggregated forms can explain t
 he well-documented stereotypical spread of disease pathology in neurodegen
 erative disorders such as Huntington’s\, Lou Gehrig’s\, Alzheimer’s 
 and Parkinson’s diseases.  I will present data demonstrating that fibril
 lar polyglutamine aggregates like those associated with Huntington’s dis
 ease can be internalized by mammalian cells in culture where they gain acc
 ess to the cytosolic compartment and become co-sequestered in aggresomes t
 ogether with components of the ubiquitin-proteasome system and cytoplasmic
  chaperones.  I will also present recent unpublished data examining the bi
 ochemical and biophysical properties of protein aggregates and cell membra
 nes that are necessary for cytoplasmic intrusion of aggregates and the imp
 lications for the pathogenesis and management of this class of conformatio
 nal disease. 
LOCATION:Max Perutz Lecture Theatre\, Medical Research Council (MRC) (MRC 
 Laboratory of Molecular Biol
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