ArticleOncogene2004
Disruption of the Rad9/Rad1/Hus1 (9-1-1) complex leads to checkpoint signaling and replication defects.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 72 citations in OpenAlex.
- Eugenol as a potential adjuvant therapy for gingival squamous cell carcinoma.Scientific reports · 2024Article
- Rad1 attenuates DNA double-strand breaks and cell cycle arrest in type II alveolar epithelial cells of rats with bronchopulmonary dysplasia.Molecular medicine (Cambridge, Mass.) · 2023Article
- ATR Inhibitors in Platinum-Resistant Ovarian Cancer.Cancers · 2022Review
- Preservation of lagging strand integrity at sites of stalled replication by Pol α-primase and 9-1-1 complex.Science advances · 2021Article
- The fission yeast FHIT homolog affects checkpoint control of proliferation and is regulated by mitochondrial electron transport.Cell biology international · 2020Article
- Combined treatment with emodin and a telomerase inhibitor induces significant telomere damage/dysfunction and cell death.Cell death & disease · 2019Article
- Functional compartmentalization of Rad9 and Hus1 reveals diverse assembly of the 9-1-1 complex components during the DNA damage response in Leishmania.Molecular microbiology · 2016Article
- TLK1B mediated phosphorylation of Rad9 regulates its nuclear/cytoplasmic localization and cell cycle checkpoint.BMC molecular biology · 2016Article
- HERC2-USP20 axis regulates DNA damage checkpoint through Claspin.Nucleic acids research · 2014Article
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
- NF-kappa B mediated up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia.Molecular cancer · 2014Article
- A molecular mechanism for therapeutic effects of cGMP-elevating agents in pulmonary arterial hypertension.The Journal of biological chemistry · 2013Article
- Role of the checkpoint clamp in DNA damage response.Biomolecules · 2013Article
- The RAD9-RAD1-HUS1 (9.1.1) complex interacts with WRN and is crucial to regulate its response to replication fork stalling.Oncogene · 2012Article
- ATM-dependent phosphorylation of the checkpoint clamp regulates repair pathways and maintains genomic stability.Cell cycle (Georgetown, Tex.) · 2012Article
- Contributions of Rad9 to tumorigenesis.Journal of cellular biochemistry · 2012Review
- Targeted deletion of mouse Rad1 leads to deficient cellular DNA damage responses.Protein & cell · 2011Article
- Differential hRad17 expression by histologic subtype of ovarian cancer.Journal of ovarian research · 2011Article
- RMI1 attenuates tumor development and is essential for early embryonic survival.Molecular carcinogenesis · 2011Article
- Human RAD18 interacts with ubiquitylated chromatin components and facilitates RAD9 recruitment to DNA double strand breaks.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The checkpoint sliding-clamp complex, Rad9/Rad1/Hus1, plays a critical role during initiation of checkpoint signals in response to DNA damage and replication disruption. We investigated the impact of loss of Rad1 on checkpoint function and on DNA replication in mammalian cells. We show that RAD1 is an essential gene for sustained cell proliferation and that loss of Rad1 causes destabilization of Rad9 and Hus1 and consequently disintegration of the sliding-clamp complex. In Rad1-depleted cells, Atr-dependent Chk1 activation was impaired whereas Atm-mediated Chk2 activation was unaffected, suggesting that the sliding clamp is required primarily in Atr-dependent signal activation. Disruption of sliding-clamp function also caused a major defect in S-phase control. Rad1-depleted cells exhibited an RDS phenotype, indicating that damage-induced S-phase arrest was compromised by Rad1 loss. Furthermore, lack of Rad1 also affected the efficiency of replication recovery from DNA synthesis blockage, resulting in a prolonged S phase. These deficiencies may perpetually generate DNA strand breakage as we have found chromosomal abnormalities in Rad1-depleted cells. We conclude that the Rad9/Rad1/Hus1 complex is essential for Atr-dependent checkpoint signaling, which may play critical roles in the facilitation of DNA replication and in the maintenance of genomic integrity.
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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.