Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury. - Wikidata - wikimedia - TriplyDB

Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury.

Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury.

http://www.wikidata.org/entity/Q36089330

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Defective DNA ligation during short-patch single-strand break repair in ataxia oculomotor apraxia 1 The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease Balancing self-renewal against genome preservation in stem cells: How do they manage to have the cake and eat it too?Base excision repair p53 coordinates base excision repair to prevent genomic instability Age- and tissue-specific changes in mitochondrial and nuclear DNA base excision repair activity in mice: Susceptibility of skeletal muscles to oxidative injury.Cyclin-C-dependent cell-cycle entry is required for activation of non-homologous end joining DNA repair in postmitotic neurons Telomeres shorten in response to oxidative stress in mouse skeletal muscle fibers Redox or death: checking on fetal myogenesis.DNA repair deficiency in neurodegeneration.DNA polymerase beta-catalyzed-PCNA independent long patch base excision repair synthesis: a mechanism for repair of oxidatively damaged DNA ends in post-mitotic brain.DNA repair kinetics in SCID mice Sertoli cells and DNA-PKcs-deficient mouse embryonic fibroblasts.Deficiency in repair of the mitochondrial genome sensitizes proliferating myoblasts to oxidative damage Creating a monomeric endonuclease TALE-I-SceI with high specificity and low genotoxicity in human cells.Irreparable complex DNA double-strand breaks induce chromosome breakage in organotypic three-dimensional human lung epithelial cell culture Human monocytes are severely impaired in base and DNA double-strand break repair that renders them vulnerable to oxidative stress Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.The nucleotide sequence, DNA damage location, and protein stoichiometry influence the base excision repair outcome at CAG/CTG repeats Quiescent keratocytes fail to repair MMC induced DNA damage leading to the long-term inhibition of myofibroblast differentiation and wound healing Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan.Alcohol-induced one-carbon metabolism impairment promotes dysfunction of DNA base excision repair in adult brain.Base excision repair, aging and health span.XRCC1 protects against the lethality of induced oxidative DNA damage in nondividing neural cells Broad DNA repair responses in neural injury are associated with activation of the IL-6 pathway in cholesterol-fed rabbits.miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells Checkpoint kinase phosphorylation in response to endogenous oxidative DNA damage in repair-deficient stationary-phase Saccharomyces cerevisiae DNA damage-activated ABL-MyoD signaling contributes to DNA repair in skeletal myoblasts.Myostatin induces DNA damage in skeletal muscle of streptozotocin-induced type 1 diabetic mice.The bright and the dark sides of DNA repair in stem cells.The role of DNA base excision repair in brain homeostasis and disease.The impact of base excision DNA repair in age-related neurodegenerative diseases HIRA deficiency in muscle fibers causes hypertrophy and susceptibility to oxidative stress.mESC-based in vitro differentiation models to study vascular response and functionality following genotoxic insults.Risky repair: DNA-protein crosslinks formed by mitochondrial base excision DNA repair enzymes acting on free radical lesions.Modulation of DNA base excision repair during neuronal differentiation.Coordination of cell cycle, DNA repair and muscle gene expression in myoblasts exposed to genotoxic stress.DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy.Temporal activation of XRCC1-mediated DNA repair is essential for muscle differentiation.c-Fos-dependent miR-22 targets MDC1 and regulates DNA repair in terminally differentiated cells.DNA damage response by single-strand breaks in terminally differentiated muscle cells and the control of muscle integrity

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Terminally differentiated muscle cells are defective in base excision DNA repair and hypersensitive to oxygen injury.

http://www.wikidata.org/entity/Q36089330

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2007 nî lūn-bûn

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2007年の論文

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Terminally differentiated musc ...... persensitive to oxygen injury.

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Terminally differentiated musc ...... persensitive to oxygen injury.

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Terminally differentiated musc ...... persensitive to oxygen injury.

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

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Terminally differentiated musc ...... ypersensitive to oxygen injury

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Bruce Demple

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Eugenia Dogliotti

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Laura Narciso

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Mathilde Frechet

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Paolo Degan

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Pingfang Liu

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P2860

Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy-1

The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates

Chk2 mediates stabilization of the FoxM1 transcription factor to stimulate expression of DNA repair genes

An interaction between the mammalian DNA repair protein XRCC1 and DNA ligase III

Impaired nucleotide excision repair upon macrophage differentiation is corrected by E1 ubiquitin-activating enzyme

Megabase chromatin domains involved in DNA double-strand breaks in vivo

Base damage and single-strand break repair: mechanisms and functional significance of short- and long-patch repair subpathways

Terminally differentiated human neurons repair transcribed genes but display attenuated global DNA repair and modulation of repair gene expression.

Myogenic satellite cells: physiology to molecular biology.

Involvement of XRCC1 and DNA ligase III gene products in DNA base excision repair.

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104

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Annapaola Franchitto

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Deborah Pajalunga

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2007-10-16T00:00:00Z

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5905564

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17940040

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2040456

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