The mitochondrial permeability transition pore in motor neurons: Involvement in the pathobiology of ALS mice
- 9 March 2009
- journal article
- Published by Elsevier BV in Experimental Neurology
- Vol. 218 (2), 333-346
- https://doi.org/10.1016/j.expneurol.2009.02.015
Abstract
No abstract availableKeywords
This publication has 100 references indexed in Scilit:
- Cyclophilin D is expressed predominantly in mitochondria of γ‐aminobutyric acidergic interneuronsJournal of Neuroscience Research, 2008
- Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's diseaseNature Medicine, 2008
- Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophyNature Medicine, 2008
- Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondriaProceedings of the National Academy of Sciences, 2008
- Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosisProceedings of the National Academy of Sciences, 2007
- Familial ALS-superoxide dismutases associate with mitochondria and shift their redox potentialsProceedings of the National Academy of Sciences, 2006
- Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemiaProceedings of the National Academy of Sciences, 2005
- Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell deathNature, 2005
- Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell deathNature, 2005
- Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosisNature, 1993