Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease
Published 2013 View Full Article
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Title
Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease
Authors
Keywords
Huntington’s disease, Huntingtin, Mitochondria dysfunction, Oxidative stress, Mitochondria permeability transition pore, Striatal cells, Mitochondrial fragmentation
Journal
Molecular Neurodegeneration
Volume 8, Issue 1, Pages 45
Publisher
Springer Nature
Online
2013-12-12
DOI
10.1186/1750-1326-8-45
References
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Note: Only part of the references are listed.- Impaired Mitochondrial Dynamics and Nrf2 Signaling Contribute to Compromised Responses to Oxidative Stress in Striatal Cells Expressing Full-Length Mutant Huntingtin
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- p53 Opens the Mitochondrial Permeability Transition Pore to Trigger Necrosis
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- Metabolic State Determines Sensitivity to Cellular Stress in Huntington Disease: Normalization by Activation of PPARγ
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- (2010) Andrew B. Knott et al. Annals of the New York Academy of Sciences
- Mitochondrial fission and cristae disruption increase the response of cell models of Huntington's disease to apoptotic stimuli
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- Mitochondrial calcium uptake capacity as a therapeutic target in the R6/2 mouse model of Huntington's disease
- (2010) Giselle M. Perry et al. HUMAN MOLECULAR GENETICS
- Mitochondrial loss, dysfunction and altered dynamics in Huntington's disease
- (2010) J. Kim et al. HUMAN MOLECULAR GENETICS
- Role of mitochondrial dysfunction in the pathogenesis of Huntington's disease
- (2009) Rodrigo A. Quintanilla et al. BRAIN RESEARCH BULLETIN
- Systematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models
- (2009) Liliana Menalled et al. NEUROBIOLOGY OF DISEASE
- Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells
- (2008) Rodrigo A. Quintanilla et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Paradoxical delay in the onset of disease caused by super-long CAG repeat expansions in R6/2 mice
- (2008) A Jennifer Morton et al. NEUROBIOLOGY OF DISEASE
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