Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species
about
Roles of DNA helicases in the maintenance of genome integrityOverexpression of TFAM or twinkle increases mtDNA copy number and facilitates cardioprotection associated with limited mitochondrial oxidative stressMaintaining 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 shiftBiochemical 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
P2860
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P2860
Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species
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
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
@zh-sg
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.
@nl
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
P2093
P2860
P50
P356
P1476
Overexpression of Twinkle-heli ...... sed by reactive oxygen species
@en
P2093
Anu Suomalainen
Carlos T Moraes
Siôn L Williams
Steffi Goffart
Thomas Boettger
P2860
P304
19408-19413
P356
10.1073/PNAS.1303046110
P407
P577
2013-11-11T00:00:00Z