Proteolytic processing of OPA1 links mitochondrial dysfunction to alterations in mitochondrial morphology. - Wikidata - wikimedia - TriplyDB

Proteolytic processing of OPA1 links mitochondrial dysfunction to alterations in mitochondrial morphology.

Proteolytic processing of OPA1 links mitochondrial dysfunction to alterations in mitochondrial morphology.

http://www.wikidata.org/entity/Q40227379

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The effect of OPA1 on mitochondrial Ca²⁺ signaling Inducible proteolytic inactivation of OPA1 mediated by the OMA1 protease in mammalian cells Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice Mutations in PYCR1 cause cutis laxa with progeroid features Dephosphorylation by calcineurin regulates translocation of Drp1 to mitochondria New insights into the role of mitochondria in aging: mitochondrial dynamics and more Fission and selective fusion govern mitochondrial segregation and elimination by autophagy Metabolic regulation of mitochondrial dynamics Mitochondrial morphology-emerging role in bioenergetics Morphological control of mitochondrial bioenergetics Quality control in mitochondria: use it, break it, fix it, trash it Mechanisms of mitochondria and autophagy crosstalk The molecular mechanisms of OPA1-mediated optic atrophy in Drosophila model and prospects for antioxidant treatment Metabolism. AMP-activated protein kinase mediates mitochondrial fission in response to energy stress.Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration.Distinct roles of the two isoforms of the dynamin-like GTPase Mgm1 in mitochondrial fusion.Mitochondrial metabolism and the control of vascular smooth muscle cell proliferation The i-AAA protease YME1L and OMA1 cleave OPA1 to balance mitochondrial fusion and fission Mitochondrial morphology in metabolic diseases Mitophagy mechanisms and role in human diseases Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: electron microscopy, tomography and oxygen consumption Mitochondrial dynamics in diabetic cardiomyopathy Heterozygous mutation of Drosophila Opa1 causes the development of multiple organ abnormalities in an age-dependent and organ-specific manner Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1 SLP-2 is required for stress-induced mitochondrial hyperfusion Mitochondrial dynamics and apoptosis The Interplay between Oncogenic Signaling Networks and Mitochondrial Dynamics.Expression of PHB2 in rat brain cortex following traumatic brain injury.Elevated hydrostatic pressure triggers release of OPA1 and cytochrome C, and induces apoptotic cell death in differentiated RGC-5 cells.Mitochondrial 'kiss-and-run': interplay between mitochondrial motility and fusion-fission dynamics.Bid-induced release of AIF from mitochondria causes immediate neuronal cell death Impaired mitochondrial transport and Parkin-independent degeneration of respiratory chain-deficient dopamine neurons in vivo Mitochondrial dynamics and motility inside living vascular endothelial cells: role of bioenergetics.Effect of electrical stimulation-induced resistance exercise on mitochondrial fission and fusion proteins in rat skeletal muscle.Proteolytic cleavage of Opa1 stimulates mitochondrial inner membrane fusion and couples fusion to oxidative phosphorylation.Mitochondrial Transfer from Wharton's Jelly Mesenchymal Stem Cell to MERRF Cybrid Reduces Oxidative Stress and Improves Mitochondrial Bioenergetics.Encephalomyopathies caused by abnormal nuclear-mitochondrial intergenomic cross-talk Mitochondrial dysfunction induces Sarm1-dependent cell death in sensory neurons Solving a 50 year mystery of a missing OPA1 mutation: more insights from the first family diagnosed with autosomal dominant optic atrophy.Mitochondrial oxidative phosphorylation compensation may preserve vision in patients with OPA1-linked autosomal dominant optic atrophy.

P2860

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P2860

Proteolytic processing of OPA1 links mitochondrial dysfunction to alterations in mitochondrial morphology.

http://www.wikidata.org/entity/Q40227379

description

2006 nî lūn-bûn

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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2006年论文

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2006年论文

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name

Proteolytic processing of OPA1 ...... s in mitochondrial morphology.

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type

label

Proteolytic processing of OPA1 ...... s in mitochondrial morphology.

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prefLabel

Proteolytic processing of OPA1 ...... s in mitochondrial morphology.

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P1433

Journal of Biological Chemistry

P1476

Proteolytic processing of OPA1 ...... s in mitochondrial morphology.

@en

P2093

Aleksandra Trifunovic

http://www.w3.org/2001/XMLSchema#string

Andreas S Reichert

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Anna Hansson

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Anne Chomyn

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Giuseppe Attardi

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Matthias F Bauer

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Ravi Jagasia

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Sabine Hofmann

http://www.w3.org/2001/XMLSchema#string

Walter Neupert

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P2860

Genetic and structural characterization of the human mitochondrial inner membrane translocase

OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28

Premature ageing in mice expressing defective mitochondrial DNA polymerase

Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis

Differential sublocalization of the dynamin-related protein OPA1 isoforms in mitochondria

Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis

Mitochondrial fusion in human cells is efficient, requires the inner membrane potential, and is mediated by mitofusins.

OPA1 requires mitofusin 1 to promote mitochondrial fusion

Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosis

Processing of Mgm1 by the rhomboid-type protease Pcp1 is required for maintenance of mitochondrial morphology and of mitochondrial DNA.

P304

37972-37979

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scholarly article

P356

10.1074/JBC.M606059200

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P433

49

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P478

281

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Johannes Wagener

Stéphane Duvezin-Caubet

Nils-Göran Larsson

P577

2006-09-26T00:00:00Z

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6791607

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17003040

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