Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
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The adipocyte-expressed forkhead transcription factor Foxc2 regulates metabolism through altered mitochondrial functionThe C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicalsThe molecular mechanisms of OPA1-mediated optic atrophy in Drosophila model and prospects for antioxidant treatmentOPA1-related auditory neuropathy: site of lesion and outcome of cochlear implantation.Heterozygous mutation of Drosophila Opa1 causes the development of multiple organ abnormalities in an age-dependent and organ-specific mannerLoss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity.Improved locus-specific database for OPA1 mutations allows inclusion of advanced clinical data.Mitochondrial oxidative phosphorylation in autosomal dominant optic atrophy.Heterozygous mutation of Opa1 in Drosophila shortens lifespan mediated through increased reactive oxygen species production.OPA1-related dominant optic atrophy is not strongly influenced by mitochondrial DNA background.Mitofusin 2 is necessary for transport of axonal mitochondria and interacts with the Miro/Milton complexVariation in OPA1 does not explain the incomplete penetrance of Leber hereditary optic neuropathy.Mitochondrial fragmentation and superoxide anion production in coronary endothelial cells from a mouse model of type 1 diabetes.Mitochondrial oxidative phosphorylation compensation may preserve vision in patients with OPA1-linked autosomal dominant optic atrophy.Mitochondrial remodeling following fission inhibition by 15d-PGJ2 involves molecular changes in mitochondrial fusion protein OPA1.Mitochondrial optic neuropathies - disease mechanisms and therapeutic strategies.Mitochondrial localization of telomeric protein TIN2 links telomere regulation to metabolic controlMitochondrial dynamics in cancer and neurodegenerative and neuroinflammatory diseases.Skeletal muscle mitochondria and aging: a review.Emerging functions of mammalian mitochondrial fusion and fission.A hypothesis to suggest that light is a risk factor in glaucoma and the mitochondrial optic neuropathies.Modeling autosomal dominant optic atrophy using induced pluripotent stem cells and identifying potential therapeutic targetsMitochondria at the synapse.Mitochondrial energetics and insulin resistance.Inherited mitochondrial optic neuropathies.Acute and late-onset optic atrophy due to a novel OPA1 mutation leading to a mitochondrial coupling defect.Mitochondrial cristae shape determines respiratory chain supercomplexes assembly and respiratory efficiencyMitochondrial OPA1, apoptosis, and heart failure.Disturbed mitochondrial dynamics and neurodegenerative disorders.Mitochondrial Dynamics and Heart Failure.Insulin Resistance and Mitochondrial Dysfunction.Secondary mtDNA defects do not cause optic nerve dysfunction in a mouse model of dominant optic atrophy.The OPA1 Gene Mutations Are Frequent in Han Chinese Patients with Suspected Optic Neuropathy.High-resolution en face images of microcystic macular edema in patients with autosomal dominant optic atrophy.OPA1 mutations impair mitochondrial function in both pure and complicated dominant optic atrophy.Altered skeletal muscle mitochondrial biogenesis but improved endurance capacity in trained OPA1-deficient mice.Impaired quality of life in growth hormone-deficient adults is independent of the altered skeletal muscle oxidative metabolism found in conditions with peripheral fatigue.Novel OPA1 missense mutation in a family with optic atrophy and severe widespread neurological disorder.OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion.Monitoring clinical progression with mitochondrial disease biomarkers.
P2860
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P2860
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@en
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@nl
type
label
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@en
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@nl
prefLabel
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@en
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@nl
P2093
P50
P356
P1433
P1476
Deficit of in vivo mitochondrial ATP production in OPA1-related dominant optic atrophy.
@en
P2093
Agostino Baruzzi
Bernd Wissinger
Bruno Barbiroli
Lora Longanesi
Piero Barboni
Simone Schimpf
Valeria Clementi
P2860
P304
P356
10.1002/ANA.20278
P577
2004-11-01T00:00:00Z