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Protein folding, disease treatment challenges: antibodies vs molecules
Key questions

Session 1: Technological challenges of studying protein folding

Moderator: Chris Dobson, University of Cambridge

arrow What methods are available to study structural details of proteins in vivo?

arrow How does mutational analysis help us to understand folding and disease?

arrow What can we learn from studying model systems?

arrow What is the link between protein folding and protein engineering and design?

 
 

Session 2: Cell biology of protein folding

Moderator: Ari Helenius, ETH-Hoenggerberg

arrow How does the cell respond to misfolded proteins?

arrow What is the role of molecular chaperones in controlling the formation and fate of folded proteins?

arrow How do covalent modifications, both co-translational and post-translational, affect protein folding?

arrow What is the role of the endoplasmic reticulum as a site of protein folding?

 
 

Session 3: Basic mechanisms of protein folding disease

Moderator: Denis Selkoe, Brigham and Women's Hospital

arrow Is progressive neuronal degeneration in protein misfolding diseases attributable to the effects of misfolded monomers, oligomers or (microscopically visible) polymers of the respective proteins?

arrow Are sequence-dependent denaturation energetics a major determinant of amyloid disease diversity?

arrow Would misfolded proteins that accumulate in the cytoplasm be expected to undergo a distinct kind of aggregation process to those in the extracellular space? How might they differ?

arrow Among the protein aggregation disorders of the brain, how similar are the structures and biophysical characteristics of the respective protein oligomers? Are they similar enough to envision a single compound that could effectively inhibit the aggregation of several different proteins (e.g. a-synuclein, amyloid b-protein, etc.)?

 
 

Session 4: Therapeutic strategies for protein folding diseases

Moderator: Fred Cohen, University of California, San Francisco

arrow If the tendency to form b-rich aggregates is a generic property of polypeptides, will there be generic inhibitors of this process that could have pharmaceutical implications?

arrow What do you think are the best systems for screening for inhibitors of aggregation and will they have the desired therapeutic effect if oligomeric aggregates are the toxic isoforms?

arrow What are the fundamental biological mechanisms underlying Ab immunization and what principles can be learned from animals and humans to make the general approach of clinical utility for neurodegenerative diseases?

arrow What are the challenges for drug discovery in aggregation diseases? What is the role of antibodies versus small molecules?

 
 
 
   
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