ArticleProceedings of the National Academy of Sciences of the United States of America2014
Epigenetic dysregulation by nickel through repressive chromatin domain disruption.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
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
27 citing papers in PubMed, 51 citations in OpenAlex.
- Nickel exposure disrupts epigenetic repression of developmental genes in mouse embryonic stem cells.Toxicology and applied pharmacology · 2026Article
- Epigenotoxicity: Decoding the epigenetic imprints of genotoxic agents and their implications for regulatory genetic toxicology.Environmental and molecular mutagenesis · 2025Review
- Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity.Nature genetics · 2025Article
- Article
- A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure.Toxicology and applied pharmacology · 2023Article
- Review
- CTCF and cohesin promote focal detachment of DNA from the nuclear lamina.Genome biology · 2022Article
- Transcriptional repression of E-cadherin in nickel-exposed lung epithelial cells mediated by loss of Sp1 binding at the promoter.Molecular carcinogenesis · 2022Article
- Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.Seminars in cancer biology · 2021Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021Review
- Evolution of DNA methylome from precancerous lesions to invasive lung adenocarcinomas.Nature communications · 2021Article
- Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020Article
- Pan-cancer analysis of somatic mutations and epigenetic alterations in insulated neighbourhood boundaries.PloS one · 2020Article
- Melatonin Antagonizes Nickel-Induced Aerobic Glycolysis by Blocking ROS-Mediated HIF-1Oxidative medicine and cellular longevity · 2020Article
- Nickel-induced transcriptional changes persist post exposure through epigenetic reprogramming.Epigenetics & chromatin · 2019Article
- Nickel exposure induces persistent mesenchymal phenotype in human lung epithelial cells through epigenetic activation of ZEB1.Molecular carcinogenesis · 2018Article
- Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells.Toxicology and applied pharmacology · 2018Article
- Nickel induces transcriptional down-regulation of DNA repair pathways in tumorigenic and non-tumorigenic lung cells.Carcinogenesis · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Investigations into the genomic landscape of histone modifications in heterochromatic regions have revealed histone H3 lysine 9 dimethylation (H3K9me2) to be important for differentiation and maintaining cell identity. H3K9me2 is associated with gene silencing and is organized into large repressive domains that exist in close proximity to active genes, indicating the importance of maintenance of proper domain structure. Here we show that nickel, a nonmutagenic environmental carcinogen, disrupted H3K9me2 domains, resulting in the spreading of H3K9me2 into active regions, which was associated with gene silencing. We found weak CCCTC-binding factor (CTCF)-binding sites and reduced CTCF binding at the Ni-disrupted H3K9me2 domain boundaries, suggesting a loss of CTCF-mediated insulation function as a potential reason for domain disruption and spreading. We furthermore show that euchromatin islands, local regions of active chromatin within large H3K9me2 domains, can protect genes from H3K9me2-spreading-associated gene silencing. These results have major implications in understanding H3K9me2 dynamics and the consequences of chromatin domain disruption during pathogenesis.
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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.