Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
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The rise of mitochondria in medicineMitochondrial Quality Control and Muscle Mass MaintenanceToward a therapy for mitochondrial diseaseImbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in miceMtu1-Mediated Thiouridine Formation of Mitochondrial tRNAs Is Required for Mitochondrial Translation and Is Involved in Reversible Infantile Liver InjuryLoss of OMA1 delays neurodegeneration by preventing stress-induced OPA1 processing in mitochondriaNovel targets for mitochondrial medicine.Dysregulated mitophagy and mitochondrial organization in optic atrophy due to OPA1 mutations.Leigh syndrome: One disorder, more than 75 monogenic causes.Mitochondrial network regulation and its potential interference with inflammatory signals in pancreatic beta cells.Restoration of Opa1-long isoform inhibits retinal injury-induced neurodegeneration.Beneficial effects of exercise on age-related mitochondrial dysfunction and oxidative stress in skeletal muscle.Physical exercise in aging human skeletal muscle increases mitochondrial calcium uniporter expression levels and affects mitochondria dynamics.Mitochondrial Dynamics Controls T Cell Fate through Metabolic Programming.Optic Atrophy 1 Is Epistatic to the Core MICOS Component MIC60 in Mitochondrial Cristae Shape Control.SLC25A46 is required for mitochondrial lipid homeostasis and cristae maintenance and is responsible for Leigh syndrome.Mitofusin 1 and optic atrophy 1 shift metabolism to mitochondrial respiration during aging.Therapeutic effects of the mitochondrial ROS-redox modulator KH176 in a mammalian model of Leigh Disease.T-Cell Intracellular Antigens and Hu Antigen R Antagonistically Modulate Mitochondrial Activity and Dynamics by Regulating Optic Atrophy 1 Gene Expression.Mitochondrial Ultrastructure Is Coupled to Synaptic Performance at Axonal Release Sites.Regulation of mitochondrial bioenergetics by the non-canonical roles of mitochondrial dynamics proteins in the heart.WBSCR16 Is a Guanine Nucleotide Exchange Factor Important for Mitochondrial Fusion.The short variant of the mitochondrial dynamin OPA1 maintains mitochondrial energetics and cristae structure.Unacylated ghrelin prevents mitochondrial dysfunction in a model of ischemia/reperfusion liver injury.OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance.Mitofusin-Dependent ER Stress Triggers Glial Dysfunction and Nervous System Degeneration in a Drosophila Model of Friedreich's Ataxia.Validating the RedMIT/GFP-LC3 Mouse Model by Studying Mitophagy in Autosomal Dominant Optic Atrophy Due to the OPA1Q285STOP MutationTowards a therapy for mitochondrial disease: an updateRapamycin rescues mitochondrial myopathy via coordinated activation of autophagy and lysosomal biogenesisThe cristae modulator Optic atrophy 1 requires mitochondrial ATP synthase oligomers to safeguard mitochondrial function
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P2860
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@ast
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@en
type
label
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@ast
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@en
prefLabel
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@ast
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models.
@en
P2093
P2860
P50
P1433
P1476
Opa1 overexpression ameliorates the phenotype of two mitochondrial disease mouse models
@en
P2093
Carlo Viscomi
Costanza Lamperti
Gabriele Civiletto
Massimo Zeviani
Raffaele Cerutti
Serena Barbaro
Tatiana Gorletta
P2860
P304
P356
10.1016/J.CMET.2015.04.016
P577
2015-06-01T00:00:00Z