ReviewFrontiers in cell and developmental biology2020
DNA-Histone Cross-Links: Formation and Repair.
Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Carbonyl stress by glyceraldehyde promotes glycation of nuclear non-muscle myosins in DNA-protein crosslink assemblies.Journal of clinical biochemistry and nutrition · 2026Article
- DNA-histone cross-link locks the nucleosome structure and disrupts its recognition and processing.Protein & cell · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Pathways and products of base excision DNA repair in Xenopus laevis eggs: contrast with human cell pathways.Nucleic acids research · 2025Article
- Translesion polymerases and DNA-protein crosslink repair shapes the cellular response to formaldehyde-induced DNA damage in ssDNA.Nucleic acids research · 2025Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Endogenous aldehyde-induced DNA-protein crosslinks are resolved by transcription-coupled repair.Nature cell biology · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Aldehyde-induced DNA-protein crosslinks- DNA damage, repair and mutagenesis.Frontiers in oncology · 2024Review
- Induction of the alternative lengthening of telomeres pathway by trapping of proteins on DNA.Nucleic acids research · 2023Article
- Bypass of Abasic Site-Peptide Cross-Links by Human Repair and Translesion DNA Polymerases.International journal of molecular sciences · 2023Article
- SPRTN-dependent DPC degradation precedes repair of damaged DNA: a proof of concept revealed by the STAR assay.Nucleic acids research · 2023Article
- Epigenetic regulation of macrophage polarization in wound healing.Burns & trauma · 2023Review
- Knockout and Inhibition of Ape1: Roles of Ape1 in Base Excision DNA Repair and Modulation of Gene Expression.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Mild phenotype of knockouts of the major apurinic/apyrimidinic endonuclease APEX1 in a non-cancer human cell line.PloS one · 2021Article
- Synthesis and polymerase bypass studies of DNA-peptide and DNA-protein conjugates.Methods in enzymology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The nucleosome is a stretch of DNA wrapped around a histone octamer. Electrostatic interactions and hydrogen bonds between histones and DNA are vital for the stable organization of nucleosome core particles, and for the folding of chromatin into more compact structures, which regulate gene expression via controlled access to DNA. As a drawback of tight association, under genotoxic stress, DNA can accidentally cross-link to histone in a covalent manner, generating a highly toxic DNA-histone cross-link (DHC). DHC is a bulky lesion that can impede DNA transcription, replication, and repair, often with lethal consequences. The chemotherapeutic agent cisplatin, as well as ionizing and ultraviolet irradiations and endogenously occurring reactive aldehydes, generate DHCs by forming either stable or transient covalent bonds between DNA and side-chain amino groups of histone lysine residues. The mechanisms of DHC repair start to unravel, and certain common principles of DNA-protein cross-link (DPC) repair mechanisms that participate in the removal of cross-linked histones from DNA have been described. In general, DPC is removed via a two-step repair mechanism. First, cross-linked proteins are degraded by specific DPC proteases or by the proteasome, relieving steric hindrance. Second, the remaining DNA-peptide cross-links are eliminated in various DNA repair pathways. Delineating the molecular mechanisms of DHC repair would help target specific DNA repair proteins for therapeutic intervention to combat tumor resistance to chemotherapy and radiotherapy.
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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.