ArticleNature communications2022
XPC-PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 19 citations in OpenAlex.
- Assessment and detection of nucleotide excision repair capability in human cells: a critical review of current functional methods.Molecular biology reports · 2026Review
- ROS-ATM-CBP axis-mediated PARP1 lactylation aggravates doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2026Article
- The Expanding Landscape of ADP-Ribosylation: Protein, DNA, RNA, and Mitochondrial Regulation.Chemical research in toxicology · 2026Review
- Stabilization of AFF1 by PARylation ensures transcriptional restart after DNA damage.Nature chemical biology · 2026Article
- PARP-2 catalytic activity drives replication-ICL repair in an allele-specific manner during germline development.PLoS genetics · 2026Article
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Glutamine metabolism and its roles in tumor radiotherapy by regulating DNA damage repair.Frontiers in cell and developmental biology · 2026Review
- PARP1 and PARylation facilitate transcription-coupled DNA repair by stabilizing the CSB-RNAPII complex.Nucleic acids research · 2025Article
- A Population-Specific PARP1 Gene Variation Modulates PARP Trapping.bioRxiv : the preprint server for biology · 2025Article
- Exposure of cells to near-infrared irradiation relaxes chromatin compaction and facilitates recognition of cyclo-butane pyrimidine dimers.Scientific reports · 2025Article
- Poly-(ADP-ribose) serves as a scaffold for the methyltransferase METTL3/14 complex in the DNA damage response.Nucleic acids research · 2025Article
- Utilization of natural products in diverse pathogeneses of diseases associated with single or double DNA strand damage repair.Chinese medicine · 2025Review
- FTO suppresses DNA repair by inhibiting PARP1.Nature communications · 2025Article
- Review
- Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells.Nature communications · 2024Article
- Cisplatin in the era of PARP inhibitors and immunotherapy.Pharmacology & therapeutics · 2024Review
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- Unscheduled DNA Synthesis at Sites of Local UV-induced DNA Damage to Quantify Global Genome Nucleotide Excision Repair Activity in Human Cells.Bio-protocol · 2023Article
- The XPA Protein-Life under Precise Control.Cells · 2022Review
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 6 countries.
Funding
Abstract
Cells employ global genome nucleotide excision repair (GGR) to eliminate a broad spectrum of DNA lesions, including those induced by UV light. The lesion-recognition factor XPC initiates repair of helix-destabilizing DNA lesions, but binds poorly to lesions such as CPDs that do not destabilize DNA. How difficult-to-repair lesions are detected in chromatin is unknown. Here, we identify the poly-(ADP-ribose) polymerases PARP1 and PARP2 as constitutive interactors of XPC. Their interaction results in the XPC-stimulated synthesis of poly-(ADP-ribose) (PAR) by PARP1 at UV lesions, which in turn enables the recruitment and activation of the PAR-regulated chromatin remodeler ALC1. PARP2, on the other hand, modulates the retention of ALC1 at DNA damage sites. Notably, ALC1 mediates chromatin expansion at UV-induced DNA lesions, leading to the timely clearing of CPD lesions. Thus, we reveal how chromatin containing difficult-to-repair DNA lesions is primed for repair, providing insight into mechanisms of chromatin plasticity during GGR.
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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.