ArticleNucleic acids research2007
The human checkpoint sensor Rad9-Rad1-Hus1 interacts with and stimulates NEIL1 glycosylase.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 73 citations in OpenAlex.
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- SIRT2 promotes base excision repair by transcriptionally activating OGG1 in an ATM/ATR-dependent manner.Nucleic acids research · 2024Article
- Enhanced thermal stability enables human mismatch-specific thymine-DNA glycosylase to catalyse futile DNA repair.PloS one · 2024Article
- Using Affinity Pulldown Assays to Study Protein-Protein Interactions of Human NEIL1 Glycosylase and the Checkpoint Protein RAD9-RAD1-HUS1 (9-1-1) Complex.Methods in molecular biology (Clifton, N.J.) · 2023Article
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- Formation and processing of DNA damage substrates for the hNEIL enzymes.Free radical biology & medicine · 2017Review
- Association of the Rad9-Rad1-Hus1 checkpoint clamp with MYH DNA glycosylase and DNA.DNA repair · 2015Article
- Regulation of NEIL1 protein abundance by RAD9 is important for efficient base excision repair.Nucleic acids research · 2015Article
- New paradigms in the repair of oxidative damage in human genome: mechanisms ensuring repair of mutagenic base lesions during replication and involvement of accessory proteins.Cellular and molecular life sciences : CMLS · 2015Review
- Increased sensitivity of DNA damage response-deficient cells to stimulated microgravity-induced DNA lesions.PloS one · 2015Article
- Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.Cellular and molecular life sciences : CMLS · 2014Review
- Hypersensitivity of mouse NEIL1-knockdown cells to hydrogen peroxide during S phase.Journal of radiation research · 2014Article
- Cockayne Syndrome group B protein stimulates NEIL2 DNA glycosylase activity.Mechanisms of ageing and development · 2014Article
- Coordination of MYH DNA glycosylase and APE1 endonuclease activities via physical interactions.DNA repair · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The checkpoint protein Rad9/Rad1/Hus1 heterotrimer (the 9-1-1 complex) is structurally similar to the proliferating cell nuclear antigen sliding clamp and has been proposed to sense DNA damage that leads to cell cycle arrest or apoptosis. Human (h) NEIL1 DNA glycosylase, an ortholog of bacterial Nei/Fpg, is involved in repairing oxidatively damaged DNA bases. In this study, we show that hNEIL1 interacts with hRad9, hRad1 and hHus1 as individual proteins and as a complex. Residues 290-350 of hNEIL1 are important for the 9-1-1 association. A significant fraction of the hNEIL1 nuclear foci co-localize with hRad9 foci in hydrogen peroxide treated cells. Human NEIL1 DNA glycosylase activity is significantly stimulated by hHus1, hRad1, hRad9 separately and the 9-1-1 complex. Thus, the 9-1-1 complex at the lesion sites serves as both a damage sensor to activate checkpoint control and a component of base excision repair.
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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.