ArticleNature communications2017
ASH1L histone methyltransferase regulates the handoff between damage recognition factors in global-genome nucleotide excision repair.
Article in Nature communications, 2017. 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.
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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
18 citing papers in PubMed, 32 citations in OpenAlex.
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Targeting Ash1L-STING Axis Restores NK Cell Function and Ameliorates Immune-Mediated Bone Marrow Failure Diseases.International journal of biological sciences · 2026Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- The histone demethylase JMJ27 acts during the UV-induced modulation of H3K9me2 landscape and facilitates photodamage repair.Nature plants · 2024Article
- ASH1L guards cis-regulatory elements against cyclobutane pyrimidine dimer induction.Nucleic acids research · 2024Article
- ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair.Nature communications · 2023Article
- Structural and functional specificity of H3K36 methylation.Epigenetics & chromatin · 2022Review
- Histone deacetylation regulates nucleotide excision repair through an interaction with the XPC protein.iScience · 2022Article
- Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022Review
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
- Collateral Victim or Rescue Worker?-The Role of Histone Methyltransferases in DNA Damage Repair and Their Targeting for Therapeutic Opportunities in Cancer.Frontiers in cell and developmental biology · 2021Review
- Formation and Recognition of UV-Induced DNA Damage within Genome Complexity.International journal of molecular sciences · 2020Review
- A chromatin scaffold for DNA damage recognition: how histone methyltransferases prime nucleosomes for repair of ultraviolet light-induced lesions.Nucleic acids research · 2020Article
- Intracellular HSP70L1 inhibits human dendritic cell maturation by promoting suppressive H3K27me3 and H2AK119Ub1 histone modifications.Cellular & molecular immunology · 2020Article
- Tackling malignant melanoma epigenetically: histone lysine methylation.Clinical epigenetics · 2018Review
- Molecular basis for damage recognition and verification by XPC-RAD23B and TFIIH in nucleotide excision repair.DNA repair · 2018Review
- Article
- Comprehensive Bioinformatics Analysis of Key Methyltransferases and Demethylases for Histone Lysines in Hepatocellular Carcinoma.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Global-genome nucleotide excision repair (GG-NER) prevents ultraviolet (UV) light-induced skin cancer by removing mutagenic cyclobutane pyrimidine dimers (CPDs). These lesions are formed abundantly on DNA wrapped around histone octamers in nucleosomes, but a specialized damage sensor known as DDB2 ensures that they are accessed by the XPC initiator of GG-NER activity. We report that DDB2 promotes CPD excision by recruiting the histone methyltransferase ASH1L, which methylates lysine 4 of histone H3. In turn, methylated H3 facilitates the docking of the XPC complex to nucleosomal histone octamers. Consequently, DDB2, ASH1L and XPC proteins co-localize transiently on histone H3-methylated nucleosomes of UV-exposed cells. In the absence of ASH1L, the chromatin binding of XPC is impaired and its ability to recruit downstream GG-NER effectors diminished. Also, ASH1L depletion suppresses CPD excision and confers UV hypersensitivity. These findings show that ASH1L configures chromatin for the effective handoff between damage recognition factors during GG-NER activity.
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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.