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Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Studies for normal function of prion protein using knockout mice under the immunological or pathophysiological stress
ABSTRACT Deletion of cellular isoform of prion protein (PrPC) increased neuronal predisposition to damage by modulating to apoptosis, and the negative consequences to oxidative stress. In vivo studies demonstrated that PrPC‐deficient mice were more prone to seizure, depression and epilepsy induction, and exhibited an extent of the cerebral damage following an ischemic challenge or viral infection. Besides, adenovirus‐mediated PrPC over‐expression reduces brain damage in rat model of cerebral ischemia. In experimental autoimmune encephalomyelitis (EAE) PrPC‐deficient mice demonstrated more aggressive disease onset a...
Source: Microbiology and Immunology - May 1, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research