2004
DOI: 10.1016/j.molbrainres.2004.02.005
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The cellular prion protein (PrPC) prevents apoptotic neuronal cell death and mitochondrial dysfunction induced by serum deprivation

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Cited by 118 publications
(83 citation statements)
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“…14 Moreover, many studies have suggested that PrP C plays a neuroprotective role in response to serum deprivation and oxidative stress in neuronal and non-neuronal cell lines. [15][16][17] In response to oxidative stress, primary neurons cultured from the brains of Prnp 0/0 mice are more susceptible to cell death than those cultured from the brains of Prnp +/+ mice. 18,19 However, the molecular mechanism related to the protective role of PrP C against oxidative stress is unclear.…”
Section: Introductionmentioning
confidence: 99%
“…14 Moreover, many studies have suggested that PrP C plays a neuroprotective role in response to serum deprivation and oxidative stress in neuronal and non-neuronal cell lines. [15][16][17] In response to oxidative stress, primary neurons cultured from the brains of Prnp 0/0 mice are more susceptible to cell death than those cultured from the brains of Prnp +/+ mice. 18,19 However, the molecular mechanism related to the protective role of PrP C against oxidative stress is unclear.…”
Section: Introductionmentioning
confidence: 99%
“…In the last few years, some possible biological functions for the cellular prion protein have been described. It has been postulated that PrP C may be involved in one or more of the following: neurotransmitter metabolism, immune cell activation [17,64], cell adhesion, signal transduction, copper metabolism, antioxidant activity, or programmed cell death [46]. Writing a review of current knowledge of the role of PrP C as a cellular protein appears to be a rather delicate task.…”
Section: Introductionmentioning
confidence: 99%
“…It was also known that mitochondrion was essential during the apoptosis of cell and the change of its function relates tightly to apoptosis (25). Some experiments in cell culture models have shown that PrP C can prevent neuronal cell apoptosis and mitochondrial dysfunction (26,27). In this work, expression of PrP on which N-linked glycosylation sites were removed induced a great reduction of the membrane potential of mitochondria compared to the wild-type PrP.…”
Section: Discussionmentioning
confidence: 60%