ReviewInternational journal of molecular sciences2011
Chromatin structure following UV-induced DNA damage-repair or death?
Review in International journal of molecular sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Exposure of cells to near-infrared irradiation relaxes chromatin compaction and facilitates recognition of cyclo-butane pyrimidine dimers.Scientific reports · 2025Article
- Social context prevents heat hormetic effects against mutagens during fish development.FEBS letters · 2025Article
- The deubiquitinase OTUB1 fosters papillary thyroid carcinoma growth through EYA1 stabilization.Journal of cellular and molecular medicine · 2021Article
- Article
- Continuous transcription initiation guarantees robust repair of all transcribed genes and regulatory regions.Nature communications · 2020Article
- Histone Deacetylase Inhibitors Dose-Dependently Switch Neutrophil Death from NETosis to Apoptosis.Biomolecules · 2019Article
- Histone Acetylation Promotes Neutrophil Extracellular Trap Formation.Biomolecules · 2019Article
- Two-in-one: UV radiation simultaneously induces apoptosis and NETosis.Cell death discovery · 2018Article
- DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus.Journal of immunology research · 2018Review
- Eyes absent gene (EYA1) is a pathogenic driver and a therapeutic target for melanoma.Oncotarget · 2017Article
- Tale of a multifaceted co-activator, hADA3: from embryogenesis to cancer and beyond.Open biology · 2016Review
- Mitotic genes are transcriptionally upregulated in the fibroblast irradiated with very low doses of UV-C.Scientific reports · 2016Article
- Nucleotide Excision Repair and Vitamin D--Relevance for Skin Cancer Therapy.International journal of molecular sciences · 2016Review
- Solar Simulated Ultraviolet Radiation Induces Global Histone Hypoacetylation in Human Keratinocytes.PloS one · 2016Article
- Design, synthesis, and characterization of nucleosomes containing site-specific DNA damage.DNA repair · 2015Review
- Chromatin dynamics: H3K4 methylation and H3 variant replacement during development and in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- A genotoxic stress-responsive miRNA, miR-574-3p, delays cell growth by suppressing the enhancer of rudimentary homolog gene in vitro.International journal of molecular sciences · 2014Article
- The role of AKT/mTOR pathway in stress response to UV-irradiation: implication in skin carcinogenesis by regulation of apoptosis, autophagy and senescence.International journal of molecular sciences · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotes, DNA is compacted into a complex structure known as chromatin. The unravelling of DNA is a crucial step in DNA repair, replication, transcription and recombination as this allows access to DNA for these processes. Failure to package DNA into the nucleosome, the individual unit of chromatin, can lead to genomic instability, driving a cell into apoptosis, senescence, or cellular proliferation. Ultraviolet (UV) radiation damage causes destabilisation of chromatin integrity. UV irradiation induces DNA damage such as photolesions and subjects the chromatin to substantial rearrangements, causing the arrest of transcription forks and cell cycle arrest. Highly conserved processes known as nucleotide and base excision repair (NER and BER) then begin to repair these lesions. However, if DNA repair fails, the cell may be forced into apoptosis. The modification of various histones as well as nucleosome remodelling via ATP-dependent chromatin remodelling complexes are required not only to repair these UV-induced DNA lesions, but also for apoptosis signalling. Histone modifications and nucleosome remodelling in response to UV also lead to the recruitment of various repair and pro-apoptotic proteins. Thus, the way in which a cell responds to UV irradiation via these modifications is important in determining its fate. Failure of these DNA damage response steps can lead to cellular proliferation and oncogenic development, causing skin cancer, hence these chromatin changes are critical for a proper response to UV-induced injury.
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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.