ArticleMolecular and cellular biology2004
Definition of a short region of XPG necessary for TFIIH interaction and stable recruitment to sites of UV damage.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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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
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.
- Association between ERCC5 gene rs17655 polymorphism and the risk of breast cancer: an updated meta-analysis.Environmental health and preventive medicine · 2026Pooled it
- Association between the ERCC5 Asp1104His polymorphism and cancer risk: a meta-analysis.PloS one · 2012Pooled it
- The interaction of XPG with TFIIH through p62 and XPD is required for the completion of nucleotide excision repair.Nucleic acids research · 2026Article
- The clinical spectrum associated with ERCC5 mutations: Is there a relationship between phenotype and genotype?Pediatric discovery · 2024Article
- Review
- XPG in the Nucleotide Excision Repair and Beyond: a study on the different functional aspects of XPG and its associated diseases.Molecular biology reports · 2022Review
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Mechanism of action of nucleotide excision repair machinery.Biochemical Society transactions · 2022Review
- Transcriptional Stress Induces Chromatin Relocation of the Nucleotide Excision Repair Factor XPG.International journal of molecular sciences · 2021Article
- Envisioning how the prototypic molecular machine TFIIH functions in transcription initiation and DNA repair.DNA repair · 2020Review
- In Situ Analysis of DNA-Protein Complex Formation upon Radiation-Induced DNA Damage.International journal of molecular sciences · 2019Review
- R-loop generation during transcription: Formation, processing and cellular outcomes.DNA repair · 2018Review
- Splice variants of the endonucleases XPF and XPG contain residual DNA repair capabilities and could be a valuable tool for personalized medicine.Oncotarget · 2018Article
- Deep phenotyping of 89 xeroderma pigmentosum patients reveals unexpected heterogeneity dependent on the precise molecular defect.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Regulation of Transcription Elongation by the XPG-TFIIH Complex Is Implicated in Cockayne Syndrome.Molecular and cellular biology · 2015Article
- Cdt2-mediated XPG degradation promotes gap-filling DNA synthesis in nucleotide excision repair.Cell cycle (Georgetown, Tex.) · 2015Article
- Association of xeroderma pigmentosum complementation group G Asp1104His polymorphism with breast cancer risk: A cumulative meta-analysis.Molecular and clinical oncology · 2014Article
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- Clinical utility gene card for: Xeroderma pigmentosum.European journal of human genetics : EJHG · 2014Review
- Yeast RAD2, a homolog of human XPG, plays a key role in the regulation of the cell cycle and actin dynamics.Biology open · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
XPG is the human endonuclease that cuts 3' to DNA lesions during nucleotide excision repair. Missense mutations in XPG can lead to xeroderma pigmentosum (XP), whereas truncated or unstable XPG proteins cause Cockayne syndrome (CS), normally yielding life spans of <7 years. One XP-G individual who had advanced XP/CS symptoms at 28 years has been identified. The genetic, biochemical, and cellular defects in this remarkable case provide insight into the onset of XP and CS, and they reveal a previously unrecognized property of XPG. Both of this individual's XPG alleles produce a severely truncated protein, but an infrequent alternative splice generates an XPG protein lacking seven internal amino acids, which can account for his very slight cellular UV resistance. Deletion of XPG amino acids 225 to 231 does not abolish structure-specific endonuclease activity. Instead, this region is essential for interaction with TFIIH and for the stable recruitment of XPG to sites of local UV damage after the prior recruitment of TFIIH. These results define a new functional domain of XPG, and they demonstrate that recruitment of DNA repair proteins to sites of damage does not necessarily lead to productive repair reactions. This observation has potential implications that extend beyond nucleotide excision repair.
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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.