ArticleCell death and differentiation2012
DNA damage response by single-strand breaks in terminally differentiated muscle cells and the control of muscle integrity.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
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- Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases.Nature reviews. Molecular cell biology · 2024Review
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- Distinct regulation of ATM signaling by DNA single-strand breaks and APE1.Nature communications · 2024Article
- Maintenance of Flap Endonucleases for Long-Patch Base Excision DNA Repair in Mouse Muscle and Neuronal Cells Differentiated In Vitro.International journal of molecular sciences · 2023Article
- Article
- Downstream events initiated by expression of FSHD-associated DUX4: Studies of nucleocytoplasmic transport, γH2AX accumulation, and Bax/Bak-dependence.Biology open · 2022Article
- Oregano Phytocomplex Induces Programmed Cell Death in Melanoma Lines via Mitochondria and DNA Damage.Foods (Basel, Switzerland) · 2020Article
- In vivo analysis of γH2AX+ cells in skeletal muscle from aged and obese humans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A requirement of Polo-like kinase 1 in murine embryonic myogenesis and adult muscle regeneration.eLife · 2019Article
- Wound-induced polyploidization is driven by Myc and supports tissue repair in the presence of DNA damage.Development (Cambridge, England) · 2019Article
- A patient-derived iPSC model revealed oxidative stress increases facioscapulohumeral muscular dystrophy-causative DUX4.Human molecular genetics · 2018Article
- Single-Strand Break End Resection in Genome Integrity: Mechanism and Regulation by APE2.International journal of molecular sciences · 2018Review
- Pharmacological targeting of HSP90 with 17-AAG induces apoptosis of myogenic cells through activation of the intrinsic pathway.Molecular and cellular biochemistry · 2018Article
- c-Fos-dependent miR-22 targets MDC1 and regulates DNA repair in terminally differentiated cells.Oncotarget · 2017Article
- Risky repair: DNA-protein crosslinks formed by mitochondrial base excision DNA repair enzymes acting on free radical lesions.Free radical biology & medicine · 2017Review
- Dynamical states, possibilities and propagation of stress signal.Scientific reports · 2017Article
- DNA Damage Response and DNA Repair in Skeletal Myocytes From a Mouse Model of Spinal Muscular Atrophy.Journal of neuropathology and experimental neurology · 2016Article
- miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells.Aging · 2016Article
- Acute Treatment of Resveratrol Alleviates Doxorubicin-Induced Myotoxicity in Aged Skeletal Muscle Through SIRT1-Dependent Mechanisms.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA single-strand breaks (SSB) formation coordinates the myogenic program, and defects in SSB repair in post-mitotic cells have been associated with human diseases. However, the DNA damage response by SSB in terminally differentiated cells has not been explored yet. Here we show that mouse post-mitotic muscle cells accumulate SSB after alkylation damage, but they are extraordinarily resistant to the killing effects of a variety of SSB-inducers. We demonstrate that, upon SSB induction, phosphorylation of H2AX occurs in myotubes and is largely ataxia telangiectasia mutated (ATM)-dependent. However, the DNA damage signaling cascade downstream of ATM is defective as shown by lack of p53 increase and phosphorylation at serine 18 (human serine 15). The stabilization of p53 by nutlin-3 was ineffective in activating the cell death pathway, indicating that the resistance to SSB inducers is due to defective p53 downstream signaling. The induction of specific types of damage is required to activate the cell death program in myotubes. Besides the topoisomerase inhibitor doxorubicin known for its cardiotoxicity, we show that the mitochondria-specific inhibitor menadione is able to activate p53 and to kill effectively myotubes. Cell killing is p53-dependent as demonstrated by full protection of myotubes lacking p53, but there is a restriction of p53-activated genes. This new information may have important therapeutic implications in the prevention of muscle cell toxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.