ArticleDNA repair2010
Interaction between human mismatch repair recognition proteins and checkpoint sensor Rad9-Rad1-Hus1.
Article in DNA repair, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- HUS1 as a Potential Therapeutic Target in Urothelial Cancer.Journal of clinical medicine · 2022Article
- ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling.Environmental and molecular mutagenesis · 2020Review
- Full-term low birth weight infants have differentially hypermethylated DNA related to immune system and organ growth: a comparison with full-term normal birth weight infants.BMC research notes · 2020Article
- SUMO-1 modification of FEN1 facilitates its interaction with Rad9-Rad1-Hus1 to counteract DNA replication stress.Journal of molecular cell biology · 2018Article
- Article
- Genome Protection by the 9-1-1 Complex Subunit HUS1 Requires Clamp Formation, DNA Contacts, and ATR Signaling-independent Effector Functions.The Journal of biological chemistry · 2015Article
- Excision of translesion synthesis errors orchestrates responses to helix-distorting DNA lesions.The Journal of cell biology · 2015Article
- Increased sensitivity of DNA damage response-deficient cells to stimulated microgravity-induced DNA lesions.PloS one · 2015Article
- OsHUS1 facilitates accurate meiotic recombination in rice.PLoS genetics · 2014Article
- Clamping down on mammalian meiosis.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- Exonuclease 1 (Exo1) is required for activating response to S(N)1 DNA methylating agents.DNA repair · 2012Article
- Contributions of Rad9 to tumorigenesis.Journal of cellular biochemistry · 2012Review
- MicroRNA gene dosage alterations and drug response in lung cancer.Journal of biomedicine & biotechnology · 2011Article
- Rad9 is required for B cell proliferation and immunoglobulin class switch recombination.The Journal of biological chemistry · 2010Article
- Structural, molecular and cellular functions of MSH2 and MSH6 during DNA mismatch repair, damage signaling and other noncanonical activities.Mutation researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In eukaryotic cells, the cell cycle checkpoint proteins Rad9, Rad1, and Hus1 form the 9-1-1 complex which is structurally similar to the proliferating cell nuclear antigen (PCNA) sliding clamp. hMSH2/hMSH6 (hMutS alpha) and hMSH2/hMSH3 (hMutS beta) are the mismatch recognition factors of the mismatch repair pathway. hMutS alpha has been shown to physically and functionally interact with PCNA. Moreover, DNA methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) treatment induces the G2/M cell cycle arrest that is dependent on the presence of hMutS alpha and hMutL alpha. In this study, we show that each subunit of the human 9-1-1 complex physically interacts with hMSH2, hMSH3, and hMSH6. The 9-1-1 complex from both humans and Schizosaccharomyces pombe can stimulate hMutS alpha binding with G/T-containing DNA. Rad9, Rad1, and Hus1 individual subunits can also stimulate the DNA binding activity of hMutS alpha. Human Rad9 and hMSH6 colocalize to nuclear foci of HeLa cells after exposure to MNNG. However, Rad9 does not form foci in MSH6 defective cells following MNNG treatment. In Rad9 knockdown untreated cells, the majority of the MSH6 is in cytoplasm. Following MNNG treatment, Rad9 knockdown cells has abnormal nuclear morphology and MSH6 is distributed around nuclear envelop. Our findings suggest that the 9-1-1 complex is a component of the mismatch repair involved in MNNG-induced damage response.
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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.