ArticleNature communications2020
Ubiquitin and TFIIH-stimulated DDB2 dissociation drives DNA damage handover in nucleotide excision repair.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 65 citations in OpenAlex.
- Identification of oxidative stress-related hub genes and immune infiltration characterization in chronic spontaneous urticaria.Molecular genetics and genomics : MGG · 2026Article
- XPA confers ability of endonucleases to act processively and to incise damaged nucleosomal DNA.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Decoding the germline genetic architecture of prostate cancer at a single cell resolution.PLoS genetics · 2025Article
- Investigation of radiation-induced DNA damage repair-related genes as diagnostic biomarkers for radiation.Journal of radiation research · 2025Article
- Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms.Cell death discovery · 2025Article
- Cellular and Molecular Mechanisms of Oxidative DNA Damage and Repair.Medicina (Kaunas, Lithuania) · 2025Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- XPC-RAD23B enhances UV-DDB binding to DNA to facilitate lesion search in nucleotide excision repair.Nucleic acids research · 2025Article
- Review
- KRAS mutants confer platinum resistance by regulating ALKBH5 posttranslational modifications in lung cancer.The Journal of clinical investigation · 2025Article
- Different germline variants in the XPA gene are associated with severe, intermediate, or mild neurodegeneration in xeroderma pigmentosum patients.PLoS genetics · 2024Article
- Sequential post-translational modifications regulate damaged DNA-binding protein DDB2 function.Journal of biochemistry · 2024Article
- The type of DNA damage response after decitabine treatment depends on the level of DNMT activity.Life science alliance · 2024Article
- The small CRL4Nature communications · 2024Article
- Transcription-coupled DNA-protein crosslink repair by CSB and CRL4Nature cell biology · 2024Article
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes.Nature communications · 2024Article
- Live-cell imaging of endogenous CSB-mScarletI as a sensitive marker for DNA-damage-induced transcription stress.Cell reports methods · 2024Article
- Detection of oxaliplatin- and cisplatin-DNA lesions requires different global genome repair mechanisms that affect their clinical efficacy.NAR cancer · 2023Article
- Function, mechanism and drug discovery of ubiquitin and ubiquitin-like modification with multiomics profiling for cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage sensors DDB2 and XPC initiate global genome nucleotide excision repair (NER) to protect DNA from mutagenesis caused by helix-distorting lesions. XPC recognizes helical distortions by binding to unpaired ssDNA opposite DNA lesions. DDB2 binds to UV-induced lesions directly and facilitates efficient recognition by XPC. We show that not only lesion-binding but also timely DDB2 dissociation is required for DNA damage handover to XPC and swift progression of the multistep repair reaction. DNA-binding-induced DDB2 ubiquitylation and ensuing degradation regulate its homeostasis to prevent excessive lesion (re)binding. Additionally, damage handover from DDB2 to XPC coincides with the arrival of the TFIIH complex, which further promotes DDB2 dissociation and formation of a stable XPC-TFIIH damage verification complex. Our results reveal a reciprocal coordination between DNA damage recognition and verification within NER and illustrate that timely repair factor dissociation is vital for correct spatiotemporal control of a multistep repair process.
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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.