ArticleMolecular and cellular biology2004
Deficiency in the nuclease activity of xeroderma pigmentosum G in mice leads to hypersensitivity to UV irradiation.
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 19 papers.
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
19 citing papers in PubMed, 41 citations in OpenAlex.
- 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
- 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
- Transcription-coupled nucleotide excision repair factors promote R-loop-induced genome instability.Molecular cell · 2014Article
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- Oxidative DNA damage and nucleotide excision repair.Antioxidants & redox signaling · 2013Review
- DNA damage drives accelerated bone aging via an NF-κB-dependent mechanism.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
- The role of DNA exonucleases in protecting genome stability and their impact on ageing.Age (Dordrecht, Netherlands) · 2012Review
- The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome.Cell cycle (Georgetown, Tex.) · 2011Article
- Alterations in DNA repair gene expression and their possible regulation in rat-liver regeneration.Genetics and molecular biology · 2011Article
- Review
- Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3beta.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- DNA-damage repair; the good, the bad, and the ugly.The EMBO journal · 2008Review
- XPG: its products and biological roles.Advances in experimental medicine and biology · 2008Review
- Nucleotide excision repair in an immunoglobulin variable gene is less efficient than in a housekeeping gene.Molecular immunology · 2007Article
- Genomic sequence of Spodoptera frugiperda Ascovirus 1a, an enveloped, double-stranded DNA insect virus that manipulates apoptosis for viral reproduction.Journal of virology · 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Xeroderma pigmentosum (XP) is a human disorder which is characterized by hypersensitivity to sunlight and elevated incidence of skin cancer. The disease is caused by mutations in genes that encode components of the nucleotide excision repair pathway. The gene product of XP complementation group G (XPG) is a structure-specific endonuclease which makes an incision 3' to DNA photoproducts and other helix-distorting DNA adducts. In addition, the XPG protein has been implicated in transcription and repair of oxidative DNA damage. Moreover, XPG is capable of cleaving R loops in vitro, a potential intermediate during immunoglobulin heavy-chain class switch recombination. Due to its multiple functions, complete elimination of XPG in mice results in severe postnatal growth defects and premature death. To understand the contribution of the XPG nuclease activity to its function in vivo, we introduced a point mutation into the mouse XPG gene which inactivates the nuclease catalytic site but leaves the remainder of the protein intact. The XPG nuclease-deficient animals develop normally and exhibit no obvious defect in class switch recombination. However, the mutant mice are hypersensitive to UV irradiation. This phenotype suggests that the nuclease activity of XPG is required only for nucleotide excision repair and that other regions of the protein perform independent functions.
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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.