The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals - Wikidata - thesis-toulmin - TriplyDB

The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

http://www.wikidata.org/entity/Q27314280

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The novel tail-anchored membrane protein Mff controls mitochondrial and peroxisomal fission in mammalian cells The connection between inner membrane topology and mitochondrial function Kinetics and specificity of paternal mitochondrial elimination in Caenorhabditis elegans.Opa1 is required for proper mitochondrial metabolism in early development C. elegans ATAD-3 is essential for mitochondrial activity and development Loss of functional OPA1 unbalances redox state: implications in dominant optic atrophy pathogenesis Furfural induces reactive oxygen species accumulation and cellular damage in Saccharomyces cerevisiae New insights into mitochondrial structure during cell death.Coenzyme Q protects Caenorhabditis elegans GABA neurons from calcium-dependent degeneration.Impaired complex IV activity in response to loss of LRPPRC function can be compensated by mitochondrial hyperfusion.Heterozygous mutation of Opa1 in Drosophila shortens lifespan mediated through increased reactive oxygen species production.A Select Subset of Electron Transport Chain Genes Associated with Optic Atrophy Link Mitochondria to Axon Regeneration in Caenorhabditis elegans Mitochondrial dysfunction confers resistance to multiple drugs in Caenorhabditis elegans Mitochondrial fragmentation leads to intracellular acidification in Caenorhabditis elegans and mammalian cells.Mitochondrial oxidative phosphorylation compensation may preserve vision in patients with OPA1-linked autosomal dominant optic atrophy.Morphological dynamics of mitochondria--a special emphasis on cardiac muscle cells.Hydrophobic analogues of rhodamine B and rhodamine 101: potent fluorescent probes of mitochondria in living C. elegans.A novel mitochondrial outer membrane protein, MOMA-1, that affects cristae morphology in Caenorhabditis elegans The small GTPase Arf1 modulates mitochondrial morphology and function The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells Secreted VAPB/ALS8 major sperm protein domains modulate mitochondrial localization and morphology via growth cone guidance receptors.Neural activity and CaMKII protect mitochondria from fragmentation in aging Caenorhabditis elegans neurons.Regulation of acid-base transporters by reactive oxygen species following mitochondrial fragmentation Mitochondrial dynamics and autophagy aid in removal of persistent mitochondrial DNA damage in Caenorhabditis elegans.Age-Related Phasic Patterns of Mitochondrial Maintenance in Adult Caenorhabditis elegans Neurons.Structural diversity of mitochondria: functional implications Inherited mitochondrial optic neuropathies.Mitochondrial DNA level, but not active replicase, is essential for Caenorhabditis elegans development.Stage-specific Proteomes from Onchocerca ochengi, Sister Species of the Human River Blindness Parasite, Uncover Adaptations to a Nodular Lifestyle.The Spectrum of Mitochondrial Ultrastructural Defects in Mitochondrial Myopathy.Phenotypic characterization and comparative transcriptomics of evolved Saccharomyces cerevisiae strains with improved tolerance to lignocellulosic derived inhibitors.The BCL-2-like protein CED-9 of C. elegans promotes FZO-1/Mfn1,2- and EAT-3/Opa1-dependent mitochondrial fusion.Maternal L-Carnitine Supplementation Improves Brain Health in Offspring from Cigarette Smoke Exposed Mothers New role of the BCL2 family of proteins in the regulation of mitochondrial dynamics.Mitochondrial involvement in cell death of non-mammalian eukaryotes.Mitochondrial division: molecular machinery and physiological functions.Mechanisms of mitochondrial fission and fusion.Dominant optic atrophy, OPA1, and mitochondrial quality control: understanding mitochondrial network dynamics.Toxicity testing of neurotoxic pesticides in Caenorhabditis elegans.Mitochondrial fusion, fission, and mitochondrial toxicity.

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

http://www.wikidata.org/entity/Q27314280

description

2008 nî lūn-bûn

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2008 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2008 թվականի փետրվարին հրատարակված գիտական հոդված

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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name

The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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type

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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JOURNAL.PGEN.1000022

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The C. elegans Opa1 homologue EAT-3 is essential for resistance to free radicals

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Alexander M van der Bliek

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

Ashley P Wright

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

Ayako Hasegawa

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Carmen A Mannella

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Erin D Newman-Smith

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Karolyn F Buttle

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Kent McDonald

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Mauro D Zappaterra

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

Takayuki Kanazawa

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

P2860

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

Control of mitochondrial morphology by a human mitofusin

Dynamin-related protein Drp1 is required for mitochondrial division in mammalian cells

Primary structure of a dynamin-related mouse mitochondrial GTPase and its distribution in brain, subcellular localization, and effect on mitochondrial morphology

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.

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

Mutations in human dynamin block an intermediate stage in coated vesicle formation

Deletion of the OPA1 gene in a dominant optic atrophy family: evidence that haploinsufficiency is the cause of disease

Gag3p, an outer membrane protein required for fission of mitochondrial tubules

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e1000022

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10.1371/JOURNAL.PGEN.1000022

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2

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5398927

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18454199

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Caenorhabditis elegans

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2265488

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