ArticleProceedings of the National Academy of Sciences of the United States of America2006
DNA nucleotide excision repair-dependent signaling to checkpoint activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
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.
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Who cites it
68 citing papers in PubMed, 115 citations in OpenAlex.
- Single nucleotide polymorphisms of nucleotide excision repair pathway are significantly associated with outcomes of platinum-based chemotherapy in lung cancer.Scientific reports · 2017Trial
- Ubiquitin signaling and the proteasome drive human DNA-protein crosslink repair.Nucleic acids research · 2023Article
- A scanning-to-incision switch in TFIIH-XPG induced by DNA damage licenses nucleotide excision repair.Nucleic acids research · 2023Article
- Genetic variants inCancer innovation · 2022Article
- Article
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
- Integrated stress response control of granulosa cell translation and proliferation during normal ovarian follicle development.Molecular human reproduction · 2021Article
- Circadian Rhythm of NER and ATR Pathways.Biomolecules · 2021Review
- Mechanisms of Genome Maintenance in Plants: Playing It Safe With Breaks and Bumps.Frontiers in genetics · 2021Review
- Evaluation of pyrrolizidine alkaloid-induced genotoxicity using metabolically competent TK6 cell lines.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Article
- ATR Kinase Activity Limits Mutagenesis and Promotes the Clonogenic Survival of Quiescent Human Keratinocytes Exposed to UVB Radiation.Photochemistry and photobiology · 2020Article
- ATR kinase inhibition sensitizes quiescent human cells to the lethal effects of cisplatin but increases mutagenesis.Mutation research · 2019Article
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- Removal of RTF2 from Stalled Replisomes Promotes Maintenance of Genome Integrity.Molecular cell · 2018Article
- Coupling between nucleotide excision repair and gene expression.RNA biology · 2018Review
- DNA damage-induced histone H1 ubiquitylation is mediated by HUWE1 and stimulates the RNF8-RNF168 pathway.Scientific reports · 2017Article
- Mechanisms of DNA damage, repair, and mutagenesis.Environmental and molecular mutagenesis · 2017Review
- The Intra-S Checkpoint Responses to DNA Damage.Genes · 2017Review
- PostExcision Events in Human Nucleotide Excision Repair.Photochemistry and photobiology · 2017Review
- Bringing It All Together: Coupling Excision Repair to the DNA Damage Checkpoint.Photochemistry and photobiology · 2017Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Eukaryotic cells respond to a variety of DNA insults by triggering a common signal transduction cascade, known as checkpoint response, which temporarily halts cell-cycle progression. Although the main players involved in the cascade have been identified, there is still uncertainty about the nature of the structures that activate these surveillance mechanisms. To understand the role of nucleotide excision repair (NER) in checkpoint activation, we analyzed the UV-induced phosphorylation of the key checkpoint proteins Chk1 and p53, in primary fibroblasts from patients with xeroderma pigmentosum (XP), Cockayne syndrome (CS), trichothiodystrophy (TTD), or UV light-sensitive syndrome. These disorders are due to defects in transcription-coupled NER (TC-NER) and/or global genome NER (GG-NER), the NER subpathways repairing the transcribed strand of active genes or the rest of the genome, respectively. We show here that in G0/G1 and G2/M phases of the cell cycle, triggering of the DNA damage cascade requires recognition and processing of the lesions by the GG-NER. Loss of TC-NER does not affect checkpoint activation. Mutations in XPD, XPB, and in TTDA, encoding subunits of the TFIIH complex, involved in both transcription and NER, impair checkpoint triggering. The only exception is represented by mutations in XPD, resulting in combined features of XP and CS (XP/CS) that lead to activation of the checkpoint cascade after UV radiation. Inhibition of RNA polymerase II transcription significantly reduces the phosphorylation of key checkpoint factors in XP/CS fibroblasts on exposure to UV damage.
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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.