ArticleProtein science : a publication of the Protein Society2005
Influence of denatured and intermediate states of folding on protein aggregation.
Article in Protein science : a publication of the Protein Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 50 citations in OpenAlex.
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- Theoretical Insights into the Biophysics of Protein Bi-stability and Evolutionary Switches.PLoS computational biology · 2016Article
- Transient β-hairpin formation in α-synuclein monomer revealed by coarse-grained molecular dynamics simulation.The Journal of chemical physics · 2015Article
- An implicit solvent coarse-grained lipid model with correct stress profile.The Journal of chemical physics · 2010Article
- Contrasting disease and nondisease protein aggregation by molecular simulation.Accounts of chemical research · 2008Review
- Protofibril assemblies of the arctic, Dutch, and Flemish mutants of the Alzheimer's Abeta1-40 peptide.Biophysical journal · 2008Article
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- Protein aggregation in silico.Trends in biotechnology · 2007Review
- Structure and dynamics of parallel beta-sheets, hydrophobic core, and loops in Alzheimer's A beta fibrils.Biophysical journal · 2007Article
- Determining the critical nucleus and mechanism of fibril elongation of the Alzheimer's Abeta(1-40) peptide.Journal of molecular biology · 2007Article
- Coarse-grained strategy for modeling protein stability in concentrated solutions. II: phase behavior.Biophysical journal · 2006Article
- Protein folding by distributed computing and the denatured state ensemble.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Protein-folding landscapes in multichain systems.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We simulate the aggregation thermodynamics and kinetics of proteins L and G, each of which self-assembles to the same alpha/beta [corrected] topology through distinct folding mechanisms. We find that the aggregation kinetics of both proteins at an experimentally relevant concentration exhibit both fast and slow aggregation pathways, although a greater proportion of protein G aggregation events are slow relative to those of found for protein L. These kinetic differences are correlated with the amount and distribution of intrachain contacts formed in the denatured state ensemble (DSE), or an intermediate state ensemble (ISE) if it exists, as well as the folding timescales of the two proteins. Protein G aggregates more slowly than protein L due to its rapidly formed folding intermediate, which exhibits native intrachain contacts spread across the protein, suggesting that certain early folding intermediates may be selected for by evolution due to their protective role against unwanted aggregation. Protein L shows only localized native structure in the DSE with timescales of folding that are commensurate with the aggregation timescale, leaving it vulnerable to domain swapping or nonnative interactions with other chains that increase the aggregation rate. Folding experiments that characterize the structural signatures of the DSE, ISE, or the transition state ensemble (TSE) under nonaggregating conditions should be able to predict regions where interchain contacts will be made in the aggregate, and to predict slower aggregation rates for proteins with contacts that are dispersed across the fold. Since proteins L and G can both form amyloid fibrils, this work also provides mechanistic and structural insight into the formation of prefibrillar species.
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