Protein misfolding is increasingly recognized as a factor in many diseases,
including cystic fibrosis, Parkinson's, Alzheimer's and atherosclerosis. M
any proteins involved in misfolding-based pathologies are membrane-associat
ed, such that the bilayer may play roles in normal and aberrant folding. It
can be argued that the in vivo partitioning of eukaryotic membrane protein
s between folding and misfolding pathways is under kinetic control. Moreove
r, the balance between these pathways can be surprisingly delicate.