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Team:Valencia/prion
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In 1982 Stanley B. Prusiner created the term “prion” (or proteinacius infectious particle) to name the exclusively proteic infectious agent responsible of the transmissible spongiform encephalopathies (TSEs), a group of mammalian neurodegenerative disorders. According with the widely supported “protein-only” model, the prion mechanism of transmissibility arise from the ability of the prion form of the protein to promote the conformational change of the normal cellular form to the infectious prion forms (Prusiner, 1998). | In 1982 Stanley B. Prusiner created the term “prion” (or proteinacius infectious particle) to name the exclusively proteic infectious agent responsible of the transmissible spongiform encephalopathies (TSEs), a group of mammalian neurodegenerative disorders. According with the widely supported “protein-only” model, the prion mechanism of transmissibility arise from the ability of the prion form of the protein to promote the conformational change of the normal cellular form to the infectious prion forms (Prusiner, 1998). | ||
| - | ===Fungal prions== | + | ===Fungal prions=== |
====Sup35p==== | ====Sup35p==== | ||
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Regulating the surface temperature on Mars using a prion switch
Prion
In 1982 Stanley B. Prusiner created the term “prion” (or proteinacius infectious particle) to name the exclusively proteic infectious agent responsible of the transmissible spongiform encephalopathies (TSEs), a group of mammalian neurodegenerative disorders. According with the widely supported “protein-only” model, the prion mechanism of transmissibility arise from the ability of the prion form of the protein to promote the conformational change of the normal cellular form to the infectious prion forms (Prusiner, 1998).
