ArticleMolecular and cellular biology2004
Identification of the XPG region that causes the onset of Cockayne syndrome by using Xpg mutant mice generated by the cDNA-mediated knock-in method.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- 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
- Human XPG nuclease structure, assembly, and activities with insights for neurodegeneration and cancer from pathogenic mutations.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- XPF-ERCC1 protects liver, kidney and blood homeostasis outside the canonical excision repair pathways.PLoS genetics · 2020Article
- Nucleotide excision repair genes shaping embryonic development.Open biology · 2019Review
- Repair protein persistence at DNA lesions characterizes XPF defect with Cockayne syndrome features.Nucleic acids research · 2018Article
- ERCC1-XPF cooperates with CTCF and cohesin to facilitate the developmental silencing of imprinted genes.Nature cell biology · 2017Article
- Non-catalytic Roles for XPG with BRCA1 and BRCA2 in Homologous Recombination and Genome Stability.Molecular cell · 2016Article
- Oxidative and energy metabolism as potential clues for clinical heterogeneity in nucleotide excision repair disorders.The Journal of investigative dermatology · 2015Review
- Modeling the study of DNA damage responses in mice.Methods in molecular biology (Clifton, N.J.) · 2015Review
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- Yeast RAD2, a homolog of human XPG, plays a key role in the regulation of the cell cycle and actin dynamics.Biology open · 2014Article
- Oxidative DNA damage and nucleotide excision repair.Antioxidants & redox signaling · 2013Review
- The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome.Cell cycle (Georgetown, Tex.) · 2011Article
- An Xpb mouse model for combined xeroderma pigmentosum and cockayne syndrome reveals progeroid features upon further attenuation of DNA repair.Molecular and cellular biology · 2009Article
- Review
- XPG: its products and biological roles.Advances in experimental medicine and biology · 2008Review
- Human RAD18 is involved in S phase-specific single-strand break repair without PCNA monoubiquitination.Nucleic acids research · 2007Article
- Adaptive stress response in segmental progeria resembles long-lived dwarfism and calorie restriction in mice.PLoS genetics · 2006Article
- Definition of a short region of XPG necessary for TFIIH interaction and stable recruitment to sites of UV damage.Molecular and cellular biology · 2004Article
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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
In addition to xeroderma pigmentosum (XP), mutations in the human XPG gene cause early onset of Cockayne syndrome (CS) in some patients (XPG/CS). The CS-causing mutations in such patients all produce truncated XPG proteins. To test the hypothesis that the CS phenotype, with characteristics such as growth retardation and a short life span in XPG/CS patients, results from C-terminal truncations, we constructed mutants with C-terminal truncations in mouse XPG (Xpg) (from residue D811 to the stop codon [XpgD811stop] and deletion of exon 15 [Xpg Delta ex15]). In the XpgD811stop and Xpg Delta ex15 mutations, the last 360 and 183 amino acids of the protein were deleted, respectively. To generate Xpg mutant mice, we devised the shortcut knock-in method by replacing genomic DNA with a mutated cDNA fragment (cDNA-mediated knock in). The control mice, in which one-half of Xpg genomic DNA fragment was replaced with a normal Xpg cDNA fragment, had a normal growth rate, a normal life span, normal sensitivity to UV light, and normal DNA repair ability, indicating that the Xpg gene partially replaced with the normal cDNA fragment retained normal functions. The XpgD811stop homozygous mice exhibited growth retardation and a short life span, but the Xpg Delta ex15 homozygous mice did not, indicating that deletion of the last 360 amino acids results in the CS phenotype but deletion of the last 183 amino acids does not. The XpgD811stop homozygous mice, however, exhibited a slightly milder CS phenotype than did the Xpg null mutant mice, indicating that the XpgD811stop protein still retains some Xpg function that affects the severity of the CS phenotype.
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