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Infectious proteins interaction with

A key ingredient to these proposals is that the infectious agent is an abnormal form of a host-encoded protein that can interact with its normal counterpart and cause it, too, to become abnormal. Considerable evidence suggests that prion protein (PrP) is the host protein that,... [Pg.139]

Fig. 6. Model of the cellular pathways involved in generation of PrP. In the infectious manifestation of prion diseases, extracellular PrP in the form of a prion particle (1) interacts with PrP on the cell surface, possibly in detergent-resistant rafts, catalyzing its conversion to PrP (2). Conversion may also occur after uptake of the proteins into an endosomal compartment (3). Once formed, some PrP c accumulates in lysosomes (4), although the protein is probably found in a number of other cellular locations as well. In familial prion disorders, mutant PrP is converted spontaneously to the PrP state via a series of biochemical intermediates, the earliest of which is a PIPLC-resistant form generated in the ER (5). Mutant PrP molecules are subsequently delivered to the cell surface, where they become detergent-insoluble (6) and then protease-resistant (7), possibly in raft domains. Steps 6 and 7 could also occur in endocytic organelles. (Reprinted with permission from Harris, 1999). Fig. 6. Model of the cellular pathways involved in generation of PrP. In the infectious manifestation of prion diseases, extracellular PrP in the form of a prion particle (1) interacts with PrP on the cell surface, possibly in detergent-resistant rafts, catalyzing its conversion to PrP (2). Conversion may also occur after uptake of the proteins into an endosomal compartment (3). Once formed, some PrP c accumulates in lysosomes (4), although the protein is probably found in a number of other cellular locations as well. In familial prion disorders, mutant PrP is converted spontaneously to the PrP state via a series of biochemical intermediates, the earliest of which is a PIPLC-resistant form generated in the ER (5). Mutant PrP molecules are subsequently delivered to the cell surface, where they become detergent-insoluble (6) and then protease-resistant (7), possibly in raft domains. Steps 6 and 7 could also occur in endocytic organelles. (Reprinted with permission from Harris, 1999).
Characterizations of oligomerization and dynamics of equine infectious anemia virus matrix protein and its interaction with membrane signaling molecule phosphatidylinositol 4,5-diphosphate. ... [Pg.501]


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Infectious

With proteins, interactions

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