ArticleThe EMBO journal2004
Physical and functional interactions between nucleotide excision repair and DNA damage checkpoint.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 112 citations in OpenAlex.
- The RPA-binding domain and the KKRK motif in Rad26ATRIP cooperate at the perturbed DNA replication fork for initiating checkpoint signalling.PLoS genetics · 2026Article
- In Vivo and In Vitro Studies Assessing the Safety of Monosodium Glutamate.Foods (Basel, Switzerland) · 2024Article
- A scanning-to-incision switch in TFIIH-XPG induced by DNA damage licenses nucleotide excision repair.Nucleic acids research · 2023Article
- Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021Article
- In-depth and 3-dimensional exploration of the budding yeast phosphoproteome.EMBO reports · 2021Article
- Regulation of UV damage repair in quiescent yeast cells.DNA repair · 2020Article
- Separable roles for Mec1/ATR in genome maintenance, DNA replication, and checkpoint signaling.Genes & development · 2018Article
- ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle.PloS one · 2016Article
- UV induced ubiquitination of the yeast Rad4-Rad23 complex promotes survival by regulating cellular dNTP pools.Nucleic acids research · 2015Article
- Article
- The rem mutations in the ATP-binding groove of the Rad3/XPD helicase lead to Xeroderma pigmentosum-Cockayne syndrome-like phenotypes.PLoS genetics · 2014Article
- Superoxide dismutase 1 acts as a nuclear transcription factor to regulate oxidative stress resistance.Nature communications · 2014Article
- Genome-wide high-resolution mapping of UV-induced mitotic recombination events in Saccharomyces cerevisiae.PLoS genetics · 2013Article
- Nucleotide excision repair in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites.DNA repair · 2013Article
- The mechanism of nucleotide excision repair-mediated UV-induced mutagenesis in nonproliferating cells.Genetics · 2013Article
- Induction of a G1-S checkpoint in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Contributions of Rad9 to tumorigenesis.Journal of cellular biochemistry · 2012Review
- Human exonuclease 1 connects nucleotide excision repair (NER) processing with checkpoint activation in response to UV irradiation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Mind the gap: keeping UV lesions in check.DNA repair · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms used by checkpoints to identify DNA lesions are poorly understood and may involve the function of repair proteins. Looking for mutants specifically defective in activating the checkpoint following UV lesions, but proficient in the response to methyl methane sulfonate and double-strand breaks, we isolated cdu1-1, which is allelic to RAD14, the homolog of human XPA, involved in lesion recognition during nucleotide excision repair (NER). Rad14 was also isolated as a partner of the Ddc1 checkpoint protein in a two-hybrid screening, and physical interaction was proven by co-immunoprecipitation. We show that lesion recognition is not sufficient for checkpoint activation, but processing, carried out by repair factors, is required for recruiting checkpoint proteins to damaged DNA. Mutations affecting the core NER machinery abolish G1 and G2 checkpoint responses to UV, preventing activation of the Mec1 kinase and its binding to chromosomes. Conversely, elimination of transcription-coupled or global genome repair alone does not affect checkpoints, suggesting a possible interpretation for the heterogeneity in cancer susceptibility observed in different NER syndrome patients.
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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.