NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease. - Wikidata - wikimedia - TriplyDB

NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease.

NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease.

http://www.wikidata.org/entity/Q33735567

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Emerging therapeutic roles for NAD(+) metabolism in mitochondrial and age-related disorders Nuclear receptors and AMPK: can exercise mimetics cure diabetes?Mitochondrial disorders in children: toward development of small-molecule treatment strategies Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity The Molecular Circadian Clock and Alcohol-Induced Liver Injury The mitochondrial unfolded protein response—synchronizing genomes Sources and implications of NADH/NAD(+) redox imbalance in diabetes and its complications Toward a therapy for mitochondrial disease PARP inhibition delays progression of mitochondrial encephalopathy in mice.New facets in the regulation of gene expression by ADP-ribosylation and poly(ADP-ribose) polymerases.Maternally transmitted mitochondrial DNA mutations can reduce lifespan Metabolic control of autophagy Mitochondrial DNA: impacting central and peripheral nervous systems.Increasing NAD synthesis in muscle via nicotinamide phosphoribosyltransferase is not sufficient to promote oxidative metabolism.NAD(+) Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus Potential compounds for the treatment of mitochondrial disease.Mitochondrial Diseases Part III: Therapeutic interventions in mouse models of OXPHOS deficiencies.Generation, Release, and Uptake of the NAD Precursor Nicotinic Acid Riboside by Human Cells Cigarette toxicity triggers Leber's hereditary optic neuropathy by affecting mtDNA copy number, oxidative phosphorylation and ROS detoxification pathways Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice.Emerging therapies for mitochondrial disorders.NAD+ Supplementation Attenuates Methylmercury Dopaminergic and Mitochondrial Toxicity in Caenorhabditis Elegans.Sirtuin activation as a therapeutic approach against inborn errors of metabolism.Mitochondrial Respiration Controls Lysosomal Function during Inflammatory T Cell Responses.Sirtuins and the circadian clock: bridging chromatin and metabolism.Metabolic effects of resveratrol: addressing the controversies.Mechanisms by which different functional states of mitochondria define yeast longevity.The human NAD metabolome: Functions, metabolism and compartmentalization.Emerging aspects of treatment in mitochondrial disorders.DNA Damage, DNA Repair, Aging, and Neurodegeneration Mutations causing mitochondrial disease: What is new and what challenges remain?Protein acetylation in metabolism - metabolites and cofactors.Leigh syndrome: One disorder, more than 75 monogenic causes.NAD(H) and NADP(H) Redox Couples and Cellular Energy Metabolism.Inhibition of Poly(ADP-ribose) Polymerase-1 Enhances Gene Expression of Selected Sirtuins and APP Cleaving Enzymes in Amyloid Beta Cytotoxicity.NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy.Emerging drugs affecting skeletal muscle function and mitochondrial biogenesis - Potential implications for sports drug testing programs.NAD and the aging process: Role in life, death and everything in between.Pharmacologic targeting of sirtuin and PPAR signaling improves longevity and mitochondrial physiology in respiratory chain complex I mutant Caenorhabditis elegans.Relief for retinal neurons under pressure.

P2860

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P2860

NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease.

http://www.wikidata.org/entity/Q33735567

description

2014 nî lūn-bûn

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2014 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2014 թվականի մայիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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J.CMET.2014.04.001

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Cell Metabolism

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NAD(+)-dependent activation of ...... odel of mitochondrial disease.

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Anthony A Sauve

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Carlo Viscomi

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Eija Pirinen

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Eric A Schon

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Françoise Dantzer

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Raffaele Cerutti

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Silvia Marchet

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Valerio Leoni

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Wei Li

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P2860

Fatal infantile cardioencephalomyopathy with COX deficiency and mutations in SCO2, a COX assembly gene

hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase

Sirtuins as regulators of metabolism and healthspan

Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase

Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans.

Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1

Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging

NAD metabolism and sirtuins: metabolic regulation of protein deacetylation in stress and toxicity

Analysis of mouse models of cytochrome c oxidase deficiency owing to mutations in Sco2

The cell-non-autonomous nature of electron transport chain-mediated longevity

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1042-1049

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10.1016/J.CMET.2014.04.001

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6

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19

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Massimo Zeviani

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2014-05-08T00:00:00Z

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262230978

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24814483

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4051987

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