ReviewInternational journal of molecular sciences2012
The heterochromatic barrier to DNA double strand break repair: how to get the entry visa.
Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
The trial behind it
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
56 citing papers in PubMed, 106 citations in OpenAlex.
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- The consequences of differential origin licensing dynamics in distinct chromatin environments.Nucleic acids research · 2022Article
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- Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage.Frontiers in cell and developmental biology · 2022Review
- Editorial: Protecting the code: DNA double-strand break repair pathway choice.Frontiers in genetics · 2022Article
- Applications of nanodosimetry in particle therapy planning and beyond.Physics in medicine and biology · 2021Review
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- Mechanisms Underlying the Suppression of Chromosome Rearrangements by Ataxia-Telangiectasia Mutated.Genes · 2021Review
- Imaging the response to DNA damage in heterochromatin domains reveals core principles of heterochromatin maintenance.Nature communications · 2021Article
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- Alpha Radiation as a Way to Target Heterochromatic and Gamma Radiation-Exposed Breast Cancer Cells.Cells · 2020Article
- SIRT6 coordinates with CHD4 to promote chromatin relaxation and DNA repair.Nucleic acids research · 2020Article
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- Correlative Light and Electron Microscopy (CLEM) Analysis of Nuclear Reorganization Induced by Clustered DNA Damage Upon Charged Particle Irradiation.International journal of molecular sciences · 2020Article
- Mathematical Model of ATM Activation and Chromatin Relaxation by Ionizing Radiation.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Over recent decades, a deep understanding of pathways that repair DNA double strand breaks (DSB) has been gained from biochemical, structural, biophysical and cellular studies. DNA non-homologous end-joining (NHEJ) and homologous recombination (HR) represent the two major DSB repair pathways, and both processes are now well understood. Recent work has demonstrated that the chromatin environment at a DSB significantly impacts upon DSB repair and that, moreover, dramatic modifications arise in the chromatin surrounding a DSB. Chromatin is broadly divided into open, transcriptionally active, euchromatin (EC) and highly compacted, transcriptionally inert, heterochromatin (HC), although these represent extremes of a spectrum. The HC superstructure restricts both DSB repair and damage response signaling. Moreover, DSBs within HC (HC-DSBs) are rapidly relocalized to the EC-HC interface. The damage response protein kinase, ataxia telangiectasia mutated (ATM), is required for HC-DSB repair but is dispensable for the relocalization of HC-DSBs. It has been proposed that ATM signaling enhances HC relaxation in the DSB vicinity and that this is a prerequisite for HC-DSB repair. Hence, ATM is essential for repair of HC-DSBs. Here, we discuss how HC impacts upon the response to DSBs and how ATM overcomes the barrier that HC poses to repair.
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What OpenQuestion holds
Registered trials
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.