Deletion of N-terminal residues 23-88 from prion protein (PrP) abrogates the potential to rescue PrP-deficient mice from PrP-like protein/doppel-induced Neurodegeneration.

Abstract

Accumulating evidence has suggested that prion protein (PrP) is neuroprotective and that a PrP-like protein/Doppel (PrPLP/Dpl) is neurotoxic. A line of PrP-deficient mice, Ngsk Prnp0/0, ectopically expressing PrPLP/Dpl in neurons, exhibits late-onset ataxia because of Purkinje cell death that is prevented by a transgene encoding wild-type mouse PrP. To… (More)

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@article{Atarashi2003DeletionON, title={Deletion of N-terminal residues 23-88 from prion protein (PrP) abrogates the potential to rescue PrP-deficient mice from PrP-like protein/doppel-induced Neurodegeneration.}, author={Ryuichiro Atarashi and Noriyuki Nishida and Kazuto Shigematsu and Shinji Goto and Takahito Kondo and Suehiro Sakaguchi and Shigeru Katamine}, journal={The Journal of biological chemistry}, year={2003}, volume={278 31}, pages={28944-9} }