After having proof of its transmissibility, the mysterious agent of human transmissible encephalopathies was considered for decades an unconventional invader. The subsequent characterization of a host amyloidogenic protein, segregating with infectivity, and the discovery of its encoding gene, led to the hypothesis that the infectious agent, termed prion, is a misfolded self-replicating protein. Prions are both infectious and neurotoxic, and recent evidence suggests that these properties segregate with distinct molecular forms of this protein. © 2005 Elsevier Ltd. All rights reserved.
Molecular mechanisms of human prion diseases
Zanusso G.;Monaco S.
2005-01-01
Abstract
After having proof of its transmissibility, the mysterious agent of human transmissible encephalopathies was considered for decades an unconventional invader. The subsequent characterization of a host amyloidogenic protein, segregating with infectivity, and the discovery of its encoding gene, led to the hypothesis that the infectious agent, termed prion, is a misfolded self-replicating protein. Prions are both infectious and neurotoxic, and recent evidence suggests that these properties segregate with distinct molecular forms of this protein. © 2005 Elsevier Ltd. All rights reserved.
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