Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis
about
Antamanide, a derivative of Amanita phalloides, is a novel inhibitor of the mitochondrial permeability transition poreCyclophilin D controls mitochondrial pore-dependent Ca(2+) exchange, metabolic flexibility, and propensity for heart failure in mice.Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for Duchenne muscular dystrophyThe Dual Function of Reactive Oxygen/Nitrogen Species in Bioenergetics and Cell Death: The Role of ATP SynthasePPARγ as a therapeutic target to rescue mitochondrial function in neurological diseaseInflammation, Iron, Energy Failure, and Oxidative Stress in the Pathogenesis of Multiple SclerosisPhosphate is essential for inhibition of the mitochondrial permeability transition pore by cyclosporin A and by cyclophilin D ablationA model of toxic neuropathy in Drosophila reveals a role for MORN4 in promoting axonal degenerationCalcium release from intra-axonal endoplasmic reticulum leads to axon degeneration through mitochondrial dysfunctionSex-dependent treatment of chronic EAE with partial MHC class II constructs.Unlocking the Door to Neuronal Woes in Alzheimer's Disease: Aβ and Mitochondrial Permeability Transition PoreAnalysis of the mitochondrial proteome in multiple sclerosis cortex.Role of mitochondria in mutant SOD1 linked amyotrophic lateral sclerosisA novel unbiased proteomic approach to detect the reactivity of cerebrospinal fluid in neurological diseasesCyclophilin D Promotes Brain Mitochondrial F1FO ATP Synthase Dysfunction in Aging Mice.Mitochondrial calcium uptake capacity as a therapeutic target in the R6/2 mouse model of Huntington's disease.Cyclophilin D-sensitive mitochondrial permeability transition in adult human brain and liver mitochondria.Review: Mitochondria and disease progression in multiple sclerosisInitiation and progression of axonopathy in experimental autoimmune encephalomyelitis.Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases.Regulation of the mPTP by SIRT3-mediated deacetylation of CypD at lysine 166 suppresses age-related cardiac hypertrophy.Enhancement of anxiety, facilitation of avoidance behavior, and occurrence of adult-onset obesity in mice lacking mitochondrial cyclophilin DA SELDI mass spectrometry study of experimental autoimmune encephalomyelitis: sample preparation, reproducibility, and differential protein expression patterns.Mitochondrial mechanisms of cell death and neuroprotection in pediatric ischemic and traumatic brain injury.Mitochondria, oligodendrocytes and inflammation in bipolar disorder: evidence from transcriptome studies points to intriguing parallels with multiple sclerosisCyclophilin D and the mitochondrial permeability transition in kidney proximal tubules after hypoxic and ischemic injuryDeletion of mitochondrial anchoring protects dysmyelinating shiverer: implications for progressive MS.Activation of the mitochondrial permeability transition pore modulates Ca2+ responses to physiological stimuli in adult neurons.Mitochondrial calcium and its regulation in neurodegeneration induced by oxidative stressIsoflurane preconditioning protects neurons from male and female mice against oxygen and glucose deprivation and is modulated by estradiol only in neurons from female mice.Axonal degeneration is mediated by the mitochondrial permeability transition pore.Human coronavirus-induced neuronal programmed cell death is cyclophilin d dependent and potentially caspase dispensable.Genetic inactivation of the p66 isoform of ShcA is neuroprotective in a murine model of multiple sclerosis.CXCR7 antagonism prevents axonal injury during experimental autoimmune encephalomyelitis as revealed by in vivo axial diffusivityMitochondrial Ca(2+) and neurodegenerationGenetic inactivation of mitochondria-targeted redox enzyme p66ShcA preserves neuronal viability and mitochondrial integrity in response to oxidative challenges.Oxidative stress inhibits axonal transport: implications for neurodegenerative diseases.The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology.Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.Lipoic acid reduces inflammation in a mouse focal cortical experimental autoimmune encephalomyelitis model.
P2860
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P2860
Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@ast
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@en
type
label
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@ast
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@en
prefLabel
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@ast
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@en
P2093
P2860
P356
P1476
Cyclophilin D inactivation pro ...... al model of multiple sclerosis
@en
P2093
Bruce G Gold
Dennis Bourdette
Dustin Johnsen
Gail Marracci
Jonathan Fowlkes
Katie Stem
Micha Rahder
Michael Forte
Priya Chaudhary
P2860
P304
P356
10.1073/PNAS.0702228104
P407
P577
2007-04-26T00:00:00Z