Metadynamics Simulation of Prion Protein: β-Structure Stability and the Early Stages of Misfolding


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Date

2006-03-01

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Journal Article

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Abstract

In the present study we have used molecular dynamics simulations to study the stability of the antiparallel β-sheet in cellular mouse prion protein (PrPC) and in the D178N mutant. In particular, using the recently developed non-Markovian metadynamics method, we have evaluated the free energy as a function of a reaction coordinate related to the β-sheet disruption/growth. We found that the antiparallel β-sheet is significantly weaker in the pathogenic D178N mutant than in the wild-type PrPC. The destabilization of PrPC β-structure in the D178N mutant is correlated to the weakening of the hydrogen bonding network involving the mutated residue, Arg164 and Tyr128 side chains. This in turn indicates that such a network apparently provides a safety mechanism for the unzipping of the antiparallel β-sheet in the PrPC. We conclude that the antiparallel β-sheet is likely to undergo disruption rather than growth under pathogenic conditions, in agreement with recent models of the misfolded monomer that assume a parallel β-helix.

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published

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128 (8)

Pages / Article No.

2705 - 2710

Publisher

American Chemical Society

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03575 - Parrinello, Michele (ehemalig) / Parrinello, Michele (former) check_circle

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