ArticleMolecular cancer2010
Mouse Rad1 deletion enhances susceptibility for skin tumor development.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Defects in DNA damage signaling and cell cycle checkpoints in a mouse model of Rhno1 deletion.Cell death discovery · 2025Article
- A Chemotherapy Response-Related Gene Signature and DNAJC8 as Key Mediators of Hepatocellular Carcinoma Progression and Drug Resistance.Journal of hepatocellular carcinoma · 2025Article
- PLA2G7/PAF-AH as Potential Negative Regulator of the Wnt Signaling Pathway Mediates Protective Effects in BRCA1 Mutant Breast Cancer.International journal of molecular sciences · 2023Article
- DNA methylation molecular subtypes for prognosis prediction in lung adenocarcinoma.BMC pulmonary medicine · 2022Article
- Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.eLife · 2022Article
- Article
- A novel DNA damage repair-related signature for predicting prognositc and treatment response in non-small lung cancer.Frontiers in oncology · 2022Article
- An Eye in the Replication Stress Response: Lessons From Tissue-Specific StudiesFrontiers in cell and developmental biology · 2021Review
- Biological roles of Yin Yang 2: Its implications in physiological and pathological events.Journal of cellular and molecular medicine · 2020Review
- ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling.Environmental and molecular mutagenesis · 2020Review
- Article
- Genome maintenance and bioenergetics of the long-lived hypoxia-tolerant and cancer-resistant blind mole rat, Spalax: a cross-species analysis of brain transcriptome.Scientific reports · 2016Article
- The Exonuclease Homolog OsRAD1 Promotes Accurate Meiotic Double-Strand Break Repair by Suppressing Nonhomologous End Joining.Plant physiology · 2016Article
- 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
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
- Clamping down on mammalian meiosis.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- JWA deficiency suppresses dimethylbenz[a]anthracene-phorbol ester induced skin papillomas via inactivation of MAPK pathway in mice.PloS one · 2012Article
- Targeted deletion of mouse Rad1 leads to deficient cellular DNA damage responses.Protein & cell · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCells are constantly exposed to stresses from cellular metabolites as well as environmental genotoxins. DNA damage caused by these genotoxins can be efficiently fixed by DNA repair in cooperation with cell cycle checkpoints. Unrepaired DNA lesions can lead to cell death, gene mutation and cancer. The Rad1 protein, evolutionarily conserved from yeast to humans, exists in cells as monomer as well as a component in the 9-1-1 protein complex. Rad1 plays crucial roles in DNA repair and cell cycle checkpoint control, but its contribution to carcinogenesis is unknown.
resultsTo address this question, we constructed mice with a deletion of Mrad1. Matings between heterozygous Mrad1 mutant mice produced Mrad1+/+ and Mrad1+/- but no Mrad1-/- progeny, suggesting the Mrad1 null is embryonic lethal. Mrad1+/- mice demonstrated no overt abnormalities up to one and half years of age. DMBA-TPA combinational treatment was used to induce tumors on mouse skin. Tumors were larger, more numerous, and appeared earlier on the skin of Mrad1+/- mice compared to Mrad1+/+ animals. Keratinocytes isolated from Mrad1+/- mice had significantly more spontaneous DNA double strand breaks, proliferated slower and had slightly enhanced spontaneous apoptosis than Mrad1+/+ control cells.
conclusionThese data suggest that Mrad1 is important for preventing tumor development, probably through maintaining genomic integrity. The effects of heterozygous deletion of Mrad1 on proliferation and apoptosis of keratinocytes is different from those resulted from Mrad9 heterozygous deletion (from our previous study), suggesting that Mrad1 also functions independent of Mrad9 besides its role in the Mrad9-Mrad1-Mhus1 complex in mouse cells.
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Registered trials
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