Abstract
A large and diverse number of diseases are now recognized as 'conformational diseases', caused by adoption of non-native protein conformations that lead to aggregation. The recent conference, 'Alpha1-antitrypsin deficiency and other conformational diseases', held in Airlie, Virginia, USA (27-30 June, 2000) focused on some of the common pathways by which cells protect themselves from toxicity associated with protein misfolding and aggregation.
MeSH terms
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Calcium-Binding Proteins / metabolism
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Calnexin
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Calreticulin
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Cystic Fibrosis Transmembrane Conductance Regulator / metabolism
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Eukaryotic Initiation Factor-2 / metabolism
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Glycogen Synthase / metabolism
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Humans
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Mannose / metabolism
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Mannosidases / metabolism
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Protein Conformation
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Protein Folding
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Protein Structure, Secondary
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Ribonucleoproteins / metabolism
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alpha 1-Antitrypsin / chemistry*
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alpha 1-Antitrypsin Deficiency / metabolism*
Substances
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CFTR protein, human
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Calcium-Binding Proteins
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Calreticulin
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Eukaryotic Initiation Factor-2
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Ribonucleoproteins
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alpha 1-Antitrypsin
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Cystic Fibrosis Transmembrane Conductance Regulator
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Calnexin
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Glycogen Synthase
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Mannosidases
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mannosyl-oligosaccharide 1,2-alpha-mannosidase
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Mannose