ArticleMolecular and cellular biology2004
Deletion of mouse rad9 causes abnormal cellular responses to DNA damage, genomic instability, and embryonic lethality.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
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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
70 citing papers in PubMed, 114 citations in OpenAlex.
- Parasitic castration by a viral protein tyrosine phosphatase targeting the host cell cycle checkpoint protein Rad9A.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Defects in DNA damage signaling and cell cycle checkpoints in a mouse model of Rhno1 deletion.Cell death discovery · 2025Article
- Knockout ofBiomedicines · 2024Article
- Exonucleases: Degrading DNA to Deal with Genome Damage, Cell Death, Inflammation and Cancer.Cells · 2022Review
- Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.eLife · 2022Article
- Article
- Hypermethylation ofEXCLI journal · 2022Article
- FOXP1 and NDRG1 act differentially as downstream effectors of RAD9-mediated prostate cancer cell functions.Cellular signalling · 2021Article
- Genes and pathways associated with pregnancy loss in dairy cattle.Scientific reports · 2021Article
- DNMT1 and DNMT3B regulate tumorigenicity of human prostate cancer cells by controlling RAD9 expression through targeted methylation.Carcinogenesis · 2021Article
- An Eye in the Replication Stress Response: Lessons From Tissue-Specific StudiesFrontiers in cell and developmental biology · 2021Review
- ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling.Environmental and molecular mutagenesis · 2020Review
- Investigation of the Possible Role of RAD9 in Post-Diapaused Embryonic Development of the Brine ShrimpGenes · 2019Article
- Rad9a is involved in chromatin decondensation and post-zygotic embryo development in mice.Cell death and differentiation · 2019Article
- The Trends in Global Gene Expression in Mouse Embryonic Stem Cells During Spaceflight.Frontiers in genetics · 2019Article
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- p53 and RAD9, the DNA Damage Response, and Regulation of Transcription Networks.Radiation research · 2017Review
- Rad9a is required for spermatogonia differentiation in mice.Oncotarget · 2016Article
- Three-dimensional microCT imaging of mouse development from early post-implantation to early postnatal stages.Developmental biology · 2016Article
- The Exonuclease Homolog OsRAD1 Promotes Accurate Meiotic Double-Strand Break Repair by Suppressing Nonhomologous End Joining.Plant physiology · 2016Article
10 more citing papers are in PubMed but not listed here.
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 fission yeast Schizosaccharomyces pombe rad9 gene promotes cell survival through activation of cell cycle checkpoints induced by DNA damage. Mouse embryonic stem cells with a targeted deletion of Mrad9, the mouse ortholog of this gene, were created to evaluate its function in mammals. Mrad9(-/-) cells demonstrated a marked increase in spontaneous chromosome aberrations and HPRT mutations, indicating a role in the maintenance of genomic integrity. These cells were also extremely sensitive to UV light, gamma rays, and hydroxyurea, and heterozygotes were somewhat sensitive to the last two agents relative to Mrad9(+/+) controls. Mrad9(-/-) cells could initiate but not maintain gamma-ray-induced G(2) delay and retained the ability to delay DNA synthesis rapidly after UV irradiation, suggesting that checkpoint abnormalities contribute little to the radiosensitivity observed. Ectopic expression of Mrad9 or human HRAD9 complemented Mrad9(-/-) cell defects, indicating that the gene has radioresponse and genomic maintenance functions that are evolutionarily conserved. Mrad9(+/-) mice were generated, but heterozygous intercrosses failed to yield Mrad9(-/-) pups, since embryos died at midgestation. Furthermore, Mrad9(-/-) mouse embryo fibroblasts were not viable. These investigations establish Mrad9 as a key mammalian genetic element of pathways that regulate the cellular response to DNA damage, maintenance of genomic integrity, and proper embryonic development.
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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.