ArticleProceedings of the National Academy of Sciences of the United States of America2013
ARCH domain of XPD, an anchoring platform for CAK that conditions TFIIH DNA repair and transcription activities.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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55 citing papers in PubMed, 83 citations in OpenAlex.
- UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair.The Journal of biological chemistry · 2026Article
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- Visualization of stepwise derepression of TFIIH in global genome nucleotide excision repair.Science advances · 2026Article
- FAIMS-GPF XL-MS: crosslinking-mass spectrometry based on gas-phase fractionation.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
- Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II.Nature communications · 2026Article
- Review
- Translocation mechanism of xeroderma pigmentosum group D protein on single-stranded DNA and genetic disease etiology.Nature communications · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Article
- The molecular basis of human transcription-coupled DNA repair.Nature cell biology · 2025Review
- Long-read RNA sequencing unveils a novel cryptic exon in MNAT1 along with its full-length transcript structure in TDP-43 proteinopathy.Communications biology · 2025Article
- Review
- Article
- Cyclin-dependent kinase 7 (CDK7) inhibitors as a novel therapeutic strategy for different molecular types of breast cancer.British journal of cancer · 2024Review
- Characterization of human XPD helicase activity with single-molecule magnetic tweezers.Biophysical journal · 2024Article
- A Phase I Dose-Escalation Study of LY3405105, a Covalent Inhibitor of Cyclin-Dependent Kinase 7, Administered to Patients With Advanced Solid Tumors.The oncologist · 2024Article
- A Time and Cost-Effective Pipeline for Expression Screening and Protein Production in Insect Cells Based on the HR-Bac Toolbox to Generate Recombinant Baculoviruses.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Dynamic conformational switching underlies TFIIH function in transcription and DNA repair and impacts genetic diseases.Nature communications · 2023Article
- The XPA Protein-Life under Precise Control.Cells · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The xeroderma pigmentosum group D (XPD) helicase is a subunit of transcription/DNA repair factor, transcription factor II H (TFIIH) that catalyzes the unwinding of a damaged DNA duplex during nucleotide excision repair. Apart from two canonical helicase domains, XPD is composed of a 4Fe-S cluster domain involved in DNA damage recognition and a module of uncharacterized function termed the "ARCH domain." By investigating the consequences of a mutation found in a patient with trichothiodystrophy, we show that the ARCH domain is critical for the recruitment of the cyclin-dependent kinase (CDK)-activating kinase (CAK) complex. Indeed, this mutation not only affects the interaction with the MAT1 CAK subunit, thereby decreasing the in vitro basal transcription activity of TFIIH itself and impeding the efficient recruitment of the transcription machinery on the promoter of an activated gene, but also impairs the DNA unwinding activity of XPD and the nucleotide excision repair activity of TFIIH. We further demonstrate the role of CAK in downregulating the XPD helicase activity within TFIIH. Taken together, our results identify the ARCH domain of XPD as a platform for the recruitment of CAK and as a potential molecular switch that might control TFIIH composition and play a key role in the conversion of TFIIH from a factor active in transcription to a factor involved in DNA repair.
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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.