Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species - Wikidata - wikimedia - TriplyDB

Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species

Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species

http://www.wikidata.org/entity/Q37352932

about

Roles of DNA helicases in the maintenance of genome integrity Overexpression of TFAM or twinkle increases mtDNA copy number and facilitates cardioprotection associated with limited mitochondrial oxidative stress Maintaining ancient organelles: mitochondrial biogenesis and maturation.Borrowing nuclear DNA helicases to protect mitochondrial DNA.Age-Dependent Oxidative DNA Damage Does Not Correlate with Reduced Proliferation of Cardiomyocytes in Humans.Low doses of ultraviolet radiation and oxidative damage induce dramatic accumulation of mitochondrial DNA replication intermediates, fork regression, and replication initiation shift Biochemical Characterization of the Human Mitochondrial Replicative Twinkle Helicase: SUBSTRATE SPECIFICITY, DNA BRANCH MIGRATION, AND ABILITY TO OVERCOME BLOCKADES TO DNA UNWINDING.Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart.Mitochondrial DNA maintenance: an appraisal.Signaling Pathways in Cardiac Myocyte Apoptosis.Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases.Mechanistic and biological considerations of oxidatively damaged DNA for helicase-dependent pathways of nucleic acid metabolism.Cellular and population level processes influence the rate, accumulation and observed frequency of inherited and somatic mtDNA mutations.Mitochondrial Respiration Is Reduced in Atherosclerosis, Promoting Necrotic Core Formation and Reducing Relative Fibrous Cap Thickness.Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS-dependent but p53/p21-independent manner.Mitochondrial DNA repair: a novel therapeutic target for heart failure.Structural rearrangements in the mitochondrial genome of Drosophila melanogaster induced by elevated levels of the replicative DNA helicase.Twinkle overexpression prevents cardiac rupture after myocardial infarction by alleviating impaired mitochondrial biogenesis.Restoring mitochondrial DNA copy number preserves mitochondrial function and delays vascular aging in mice

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Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species

http://www.wikidata.org/entity/Q37352932

description

2013 nî lūn-bûn

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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2013年學術文章

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2013年學術文章

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name

Overexpression of Twinkle-heli ...... sed by reactive oxygen species

@en

Overexpression of Twinkle-heli ...... ed by reactive oxygen species.

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type

label

Overexpression of Twinkle-heli ...... sed by reactive oxygen species

@en

Overexpression of Twinkle-heli ...... ed by reactive oxygen species.

@nl

prefLabel

Overexpression of Twinkle-heli ...... sed by reactive oxygen species

@en

Overexpression of Twinkle-heli ...... ed by reactive oxygen species.

@nl

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PNAS.1303046110

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Proceedings of the National Academy of Sciences of the United States of America

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Overexpression of Twinkle-heli ...... sed by reactive oxygen species

@en

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Anu Suomalainen

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

Carlos T Moraes

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

Siôn L Williams

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Steffi Goffart

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Thomas Boettger

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P2860

Premature ageing in mice expressing defective mitochondrial DNA polymerase

Ubc9- and mms21-mediated sumoylation counteracts recombinogenic events at damaged replication forks.

Reactive oxygen species regulate DNA copy number in isolated yeast mitochondria by triggering recombination-mediated replication.

Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase

Twinkle helicase is essential for mtDNA maintenance and regulates mtDNA copy number

Multiple deficiencies in antioxidant enzymes in mice result in a compound increase in sensitivity to oxidative stress

Association of mitochondrial antioxidant enzymes with mitochondrial DNA as integral nucleoid constituents

Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice

Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging

High density synthetic oligonucleotide arrays

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19408-19413

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scholarly article

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10.1073/PNAS.1303046110

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110

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Jaakko Pohjoismäki

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2013-11-11T00:00:00Z

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258446174

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