Evidence map›Paper›PMID 26384665›Full record

ArticleMolecular cell2015

Tripartite DNA Lesion Recognition and Verification by XPC, TFIIH, and XPA in Nucleotide Excision Repair.

Chia-Lung Li, Filip M Golebiowski, Yuki Onishi, Nadine L Samara, Kaoru Sugasawa, Wei Yang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

92 citing papers in PubMed, 157 citations in OpenAlex.

  1. Review
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  11. Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
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  19. Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article

32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Chia-Lung LiLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Filip M GolebiowskiLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Yuki OnishiBiosignal Research Center, Organization of Advanced Science and Technology, Kobe University, Kobe 657-8501, Japan; Department of Biology, Graduate School of Science, Kobe University, Kobe 657-8501, Japan.
Nadine L SamaraLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Kaoru SugasawaBiosignal Research Center, Organization of Advanced Science and Technology, Kobe University, Kobe 657-8501, Japan; Department of Biology, Graduate School of Science, Kobe University, Kobe 657-8501, Japan.
Wei YangLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: wei.yang@nih.gov.
Kobe University · JPNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Biophysical characterization of DNA repair complex TFIIHZIADK075037 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI YANG, WEI · 2009 to 2025
$7.6M
Intramural NIH HHS ZIA DK075037NIDDK NIH HHS DK075037-06
6 · The paper itself

Abstract

Transcription factor IIH (TFIIH) is essential for both transcription and nucleotide excision repair (NER). DNA lesions are initially detected by NER factors XPC and XPE or stalled RNA polymerases, but only bulky lesions are preferentially repaired by NER. To elucidate substrate specificity in NER, we have prepared homogeneous human ten-subunit TFIIH and its seven-subunit core (Core7) without the CAK module and show that bulky lesions in DNA inhibit the ATPase and helicase activities of both XPB and XPD in Core7 to promote NER, whereas non-genuine NER substrates have no such effect. Moreover, the NER factor XPA activates unwinding of normal DNA by Core7, but inhibits the Core7 helicase activity in the presence of bulky lesions. Finally, the CAK module inhibits DNA binding by TFIIH and thereby enhances XPC-dependent specific recruitment of TFIIH. Our results support a tripartite lesion verification mechanism involving XPC, TFIIH, and XPA for efficient NER.

Indexed as

AnimalsCisplatinDNA AdductsDNA-Binding ProteinsDNA RepairDNA, Single-StrandedElectrophoretic Mobility Shift AssayHumansProtein BindingSf9 CellsSpodopteraTranscription Factor TFIIHXeroderma Pigmentosum Group A ProteinCisplatinDNA AdductsDNA-Binding ProteinsDNA, Single-StrandedTranscription Factor TFIIHXeroderma Pigmentosum Group A ProteinXPA protein, humanXPC protein, humanabasic sitecisplatinCy5motormutationWalker A motif

Identifiers

PMID26384665
PMCPMC4617536
OpenAlexW1942110646

What OpenQuestion holds

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Registered trials

None linked

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.