ArticleCell2008
XPD helicase structures and activities: insights into the cancer and aging phenotypes from XPD mutations.
Article in Cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.
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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Who cites it
237 citing papers in PubMed, 1 synthesis or guideline pooled it, 361 citations in OpenAlex.
- Xeroderma pigmentosum group D polymorphisms and esophageal cancer susceptibility: a meta-analysis based on case-control studies.World journal of gastroenterology · 2014Pooled it
- UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair.The Journal of biological chemistry · 2026Article
- Structural and biochemical characterization of a novel DinG containing an endonuclease domain.Cellular and molecular life sciences : CMLS · 2026Article
- Cryo-EM structures of human FANCJ reveal the mechanism of G-quadruplex unwinding and disease-associated mutations.Nature communications · 2026Article
- Iron-sulfur cofactors in nucleic acid metabolism and protein synthesis: Assembly, delivery, and putative roles in cellular and viral systems.The Journal of biological chemistry · 2026Review
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Base-pair scale dynamics of a repair helicase on DNA lesions reveal varied damage-sensing mechanisms.bioRxiv : the preprint server for biology · 2026Article
- G-Quadruplex Unwinding Molecular Mechanisms by Helicases and Their Applications.International journal of molecular sciences · 2026Review
- A new crystal form of the DNA-free full-length XPD helicase from Thermoplasma acidophilum.Acta crystallographica. Section F, Structural biology communications · 2026Article
- Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II.Nature communications · 2026Article
- Translocation mechanism of xeroderma pigmentosum group D protein on single-stranded DNA and genetic disease etiology.Nature communications · 2025Article
- CHIR99021 Enhances the Proliferation of Mouse Female Germline Stem Cells Via Modulating ERCC2.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Article
- Article
- Molecular model of TFIIH recruitment to the transcription-coupled repair machinery.Nature communications · 2025Article
- Review
- A gate-clamp mechanism for ssDNA translocation by DdmD in Vibrio cholerae plasmid defense.Nucleic acids research · 2025Article
- Role of Oxidative Stress in the Occurrence, Development, and Treatment of Breast Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Structure, function and evolution of the bacterial DinG-like proteins.Computational and structural biotechnology journal · 2025Review
- Molecular architecture and functional dynamics of the pre-incision complex in nucleotide excision repair.Nature communications · 2024Article
177 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in XPD helicase, required for nucleotide excision repair (NER) as part of the transcription/repair complex TFIIH, cause three distinct phenotypes: cancer-prone xeroderma pigmentosum (XP), or aging disorders Cockayne syndrome (CS), and trichothiodystrophy (TTD). To clarify molecular differences underlying these diseases, we determined crystal structures of the XPD catalytic core from Sulfolobus acidocaldarius and measured mutant enzyme activities. Substrate-binding grooves separate adjacent Rad51/RecA-like helicase domains (HD1, HD2) and an arch formed by 4FeS and Arch domains. XP mutations map along the HD1 ATP-binding edge and HD2 DNA-binding channel and impair helicase activity essential for NER. XP/CS mutations both impair helicase activity and likely affect HD2 functional movement. TTD mutants lose or retain helicase activity but map to sites in all four domains expected to cause framework defects impacting TFIIH integrity. These results provide a foundation for understanding disease consequences of mutations in XPD and related 4Fe-4S helicases including FancJ.
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What OpenQuestion holds
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.