ArticleCell cycle (Georgetown, Tex.)2015
Cdt2-mediated XPG degradation promotes gap-filling DNA synthesis in nucleotide excision repair.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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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.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Stability of c-Myc Protein in Early S Phase Is Regulated by the Interaction with PCNA.International journal of molecular sciences · 2026Article
- Noise Stress Abrogates Structure-Specific Endonucleases within the Mammalian Inner Ear.International journal of molecular sciences · 2024Article
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Transcriptional Stress Induces Chromatin Relocation of the Nucleotide Excision Repair Factor XPG.International journal of molecular sciences · 2021Article
- Regulation of DNA Replication Licensing and Re-Replication by Cdt1.International journal of molecular sciences · 2021Review
- CRL4AOncogene · 2021Article
- CRL4Cdt2 ubiquitin ligase regulates Dna2 and Rad16 (XPF) nucleases by targeting Pxd1 for degradation.PLoS genetics · 2020Article
- Review
- The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Direct binding of Cdt2 to PCNA is important for targeting the CRL4Life science alliance · 2018Article
- Screening and identification of critical transcription factors involved in the protection of cardiomyocytes against hydrogen peroxide-induced damage by Yixin-shu.Scientific reports · 2017Article
- UV radiation-induced SUMOylation of DDB2 regulates nucleotide excision repair.Carcinogenesis · 2017Article
- Forging Ahead through Darkness: PCNA, Still the Principal Conductor at the Replication Fork.Molecular cell · 2017Review
- PostExcision Events in Human Nucleotide Excision Repair.Photochemistry and photobiology · 2017Review
- Transcriptional and Posttranslational Regulation of Nucleotide Excision Repair: The Guardian of the Genome against Ultraviolet Radiation.International journal of molecular sciences · 2016Review
- Differential DNA lesion formation and repair in heterochromatin and euchromatin.Carcinogenesis · 2016Article
- TRAIP promotes DNA damage response during genome replication and is mutated in primordial dwarfism.Nature genetics · 2016Article
- Sequential replication-coupled destruction at G1/S ensures genome stability.Genes & development · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Xeroderma pigmentosum group G (XPG) protein is a structure-specific repair endonuclease, which cleaves DNA strands on the 3' side of the DNA damage during nucleotide excision repair (NER). XPG also plays a crucial role in initiating DNA repair synthesis through recruitment of PCNA to the repair sites. However, the fate of XPG protein subsequent to the excision of DNA damage has remained unresolved. Here, we show that XPG, following its action on bulky lesions resulting from exposures to UV irradiation and cisplatin, is subjected to proteasome-mediated proteolytic degradation. Productive NER processing is required for XPG degradation as both UV and cisplatin treatment-induced XPG degradation is compromised in NER-deficient XP-A, XP-B, XP-C, and XP-F cells. In addition, the NER-related XPG degradation requires Cdt2, a component of an E3 ubiquitin ligase, CRL4(Cdt2). Micropore local UV irradiation and in situ Proximity Ligation assays demonstrated that Cdt2 is recruited to the UV-damage sites and interacts with XPG in the presence of PCNA. Importantly, Cdt2-mediated XPG degradation is crucial to the subsequent recruitment of DNA polymerase δ and DNA repair synthesis. Collectively, our data support the idea of PCNA recruitment to damage sites which occurs in conjunction with XPG, recognition of the PCNA-bound XPG by CRL4(Cdt2) for specific ubiquitylation and finally the protein degradation. In essence, XPG elimination from DNA damage sites clears the chromatin space needed for the subsequent recruitment of DNA polymerase δ to the damage site and completion of gap-filling DNA synthesis during the final stage of NER.
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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.