The Journal of Neuroscience, March 30, 2005, ():
Neurodegenerative Illness in Transgenic Mice Expressing a Transmembrane Form of the Prion Protein
J. Neurosci. Stewart et al.
25: 3469
Supplemental data
Files in this Data Supplement:
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SUPPLEMENTAL FIGURE 1: Two models for the neurotoxic effect of CtmPrP, and its dependence on SecPrP. (A) CtmPrP and SecPrP physically interact to produce a neurotoxic signal. In the absence of SecPrP, CtmPrP is non-toxic. (B) SecPrP normally interacts with a molecule, Tr, that transduces a non-essential neuroprotective signal (left). When CtmPrP as well as SecPrP bind to Tr, the latter changes to an alternate conformation, Tr*, which transduces a neurotoxic signal (right). Binding of CtmPrP to Tr in the absence of SecPrP does not produce any signal. In both A and B, SecPrP is derived either from endogenous, wild-type PrP, and/or from transgenically encoded, mutant PrP.
