ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2017
Nucleosome remodelling, DNA repair and transcriptional regulation build negative feedback loops in cancer and cellular ageing.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
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- The Negative Feedback of the Glutamine/Prostatitis Loop Identified Among 1400 Metabolites and Prostatitis via Mendelian Randomization.Mediators of inflammation · 2025Article
- Single-cell histone chaperones patterns guide intercellular communication of tumor microenvironment that contribute to breast cancer metastases.Cancer cell international · 2023Article
- Molecular Mechanisms for the Regulation of Nuclear Membrane Integrity.International journal of molecular sciences · 2023Review
- A multi-scale map of protein assemblies in the DNA damage response.Cell systems · 2023Article
- Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- The Effect of the Histone Chaperones HSPA8 and DEK on Tumor Immunity in Hepatocellular Carcinoma.International journal of molecular sciences · 2023Article
- The Emerging Role of Chromatin Remodeling Complexes in Ovarian Cancer.International journal of molecular sciences · 2022Review
- Parvovirus nonstructural protein 2 interacts with chromatin-regulating cellular proteins.PLoS pathogens · 2022Article
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
- Overarching control of autophagy and DNA damage response by CHD6 revealed by modeling a rare human pathology.Nature communications · 2021Article
- Article
- Bromodomain proteins: repairing DNA damage within chromatin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- DNA repair goes hip-hop: SMARCA and CHD chromatin remodellers join the break dance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Chromatin modifiers and remodellers in DNA repair and signalling.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleosome remodelling (NR) regulates transcription in an ATP-dependent manner, and influences gene expression required for development and cellular functions, including those involved in anti-cancer and anti-ageing processes. ATP-utilizing chromatin assembly and remodelling factor (ACF) and Brahma-associated factor (BAF) complexes, belonging to the ISWI and SWI/SNF families, respectively, are involved in various types of DNA repair. Suppression of several BAF factors makes U2OS cells significantly sensitive to X-rays, UV and especially to cisplatin, and these BAF factors contribute to the accumulation of repair proteins at various types of DNA damage and to DNA repair. Recent cancer genome sequencing and expression analysis has shown that BAF factors are frequently mutated or, more frequently, silenced in various types of cancer cells. Thus, those cancer cells are potentially X-ray- and especially cisplatin-sensitive, suggesting a way of optimizing current cancer therapy. Recent single-stem cell analysis suggests that mutations and epigenetic changes influence stem cell functionality leading to cellular ageing. Genetic and epigenetic changes in the BAF factors diminish DNA repair as well as transcriptional regulation activities, and DNA repair defects in turn negatively influence NR and transcriptional regulation. Thus, they build negative feedback loops, which accelerate both cellular senescence and transformation as common and rare cellular events, respectively, causing cellular ageing.This article is part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and signalling'.
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