ArticleDNA repair2013
NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
- Article
- The RPA-binding domain and the KKRK motif in Rad26ATRIP cooperate at the perturbed DNA replication fork for initiating checkpoint signalling.PLoS genetics · 2026Article
- Mutational signature-based identification of DNA repair deficient gastroesophageal adenocarcinomas for therapeutic targeting.NPJ precision oncology · 2024Article
- UV-induced G4 DNA structures recruit ZRF1 which prevents UV-induced senescence.Nature communications · 2023Article
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
- A protein with broad functions: damage-specific DNA-binding protein 2.Molecular biology reports · 2022Review
- BAP1 promotes the repair of UV-induced DNA damage via PARP1-mediated recruitment to damage sites and control of activity and stability.Cell death and differentiation · 2022Article
- The XPA Protein-Life under Precise Control.Cells · 2022Review
- Proteomic Analysis of Nuclear Hepatitis B Virus Relaxed Circular DNA-Associated Proteins Identifies UV-Damaged DNA Binding Protein as a Host Factor Involved in Covalently Closed Circular DNA Formation.Journal of virology · 2022Article
- Xeroderma Pigmentosum Complementation Group C (XPC): Emerging Roles in Non-Dermatologic Malignancies.Frontiers in oncology · 2022Review
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
- Nuclear Receptor Coactivator NCOA3 Regulates UV Radiation-Induced DNA Damage and Melanoma Susceptibility.Cancer research · 2021Article
- Circadian Rhythm of NER and ATR Pathways.Biomolecules · 2021Review
- ATM and ATR Activation Through Crosstalk Between DNA Damage Response Pathways.Bulletin of mathematical biology · 2021Article
- DDB2 regulates DNA replication through PCNA-independent degradation of CDT2.Cell & bioscience · 2021Article
- Pharmacological Activation of Autophagy Restores Cellular Homeostasis in Ultraviolet-(B)-Induced Skin Photodamage.Frontiers in oncology · 2021Article
- Inherited Genetic Mutations and Polymorphisms in Malignant Mesothelioma: A Comprehensive Review.International journal of molecular sciences · 2020Review
- Article
- PARP1 Inhibition Augments UVB-Mediated Mitochondrial Changes-Implications for UV-Induced DNA Repair and Photocarcinogenesis.Cancers · 2019Article
- ATR kinase inhibition sensitizes quiescent human cells to the lethal effects of cisplatin but increases mutagenesis.Mutation research · 2019Article
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 1 institution in 1 country.
Funding
Abstract
ATR and ATM kinases are central to the checkpoint activation in response to DNA damage and replication stress. However, the nature of the signal, which initially activates these kinases in response to UV damage, is unclear. Here, we have shown that DDB2 and XPC, two early UV damage recognition factors, are required for the damage-specific ATR and ATM recruitment and phosphorylation. ATR and ATM physically interacted with XPC and promptly localized to the UV damage sites. ATR and ATM recruitment and their phosphorylation were negatively affected in cells defective in DDB2 or XPC functions. Consequently, the phosphorylation of ATR and ATM substrates, Chk1, Chk2, H2AX, and BRCA1 was significantly reduced or abrogated in mutant cells. Furthermore, UV exposure of cells defective in DDB2 or XPC resulted in a marked decrease in BRCA1 and Rad51 recruitment to the damage site. Conversely, ATR- and ATM-deficiency failed to affect the recruitment of DDB2 and XPC to the damage site, and therefore did not influence the NER efficiency. These findings demonstrate a novel function of DDB2 and XPC in maintaining a vital cross-talk with checkpoint proteins, and thereby coordinating subsequent repair and checkpoint activation.
Indexed as
Identifiers
What OpenQuestion holds
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.