{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360002217667357952.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1093/toxsci/kfu267"}},{"identifier":{"@type":"URI","@value":"http://academic.oup.com/toxsci/article-pdf/144/1/65/16688123/kfu267.pdf"}},{"identifier":{"@type":"PMID","@value":"25636497"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Role of p53 in the Progression from Ochratoxin A-Induced DNA Damage to Gene Mutations in the Kidneys of Mice"}],"description":[{"notation":[{"@value":"Carcinogenic doses of ochratoxin A (OTA) cause increases of mutant frequencies (MFs) of the red/gam gene (Spi(-)) in the kidneys of p53-deficient gpt delta mice, but not in p53-proficient mice. Here, we investigated the role of p53 in the progression from OTA-induced DNA damage to gene mutations. To this end, p53-proficient and -deficient mice were administered 5 mg/kg OTA for 3 days or 4 weeks by gavage. After 3 days of administration, comet assays were performed and there were no differences in the degrees of OTA-induced DNA damage between p53-proficient and -deficient mice. However, the frequencies of γ-H2AX-positive tubular epithelial cells in p53-deficient mice were significantly higher than those in p53-proficient mice, implying that p53 inhibited the progression from DNA damage to DNA double-strand breaks (DSBs). Evaluation of global gene expression and relevant mRNA/protein expression levels demonstrated that OTA increased the expression of Cdkn1a, which encodes the p21 protein, in p53-proficient mice, but not in p53-deficient mice. Moreover, in p53-deficient mice, mRNA levels of cell cycle progression and DSB repair (homologous recombination repair [HR])-related genes were significantly increased. Thus, G1/S arrest due to activation of the p53/p21 pathway may contribute to the prevention of DSBs in p53-proficient mice. In addition, single base deletions/insertions/substitutions were predominant, possibly due to HR. Overall, these results suggested that OTA induced DSBs at the carcinogenic target site in mice and that p53/p21-mediated cell cycle control prevented an increase in the formation of DSBs, leading to gene mutations."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380284920854142859","@type":"Researcher","foaf:name":[{"@value":"Ken Kuroda"}]},{"@id":"https://cir.nii.ac.jp/crid/1380284920854142856","@type":"Researcher","foaf:name":[{"@value":"Daisuke Hibi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380284920854142855","@type":"Researcher","foaf:name":[{"@value":"Yuji Ishii"}]},{"@id":"https://cir.nii.ac.jp/crid/1380284920854142857","@type":"Researcher","foaf:name":[{"@value":"Yuh 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Nohmi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380284920854142976","@type":"Researcher","foaf:name":[{"@value":"Kumiko Ogawa"}]},{"@id":"https://cir.nii.ac.jp/crid/1380284920854142852","@type":"Researcher","foaf:name":[{"@value":"Takashi Umemura"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"10960929"},{"@type":"PISSN","@value":"10966080"}],"prism:publicationName":[{"@value":"Toxicological Sciences"}],"dc:publisher":[{"@value":"Oxford University Press (OUP)"}],"prism:publicationDate":"2015-02-02","prism:volume":"144","prism:number":"1","prism:startingPage":"65","prism:endingPage":"76"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","url":[{"@id":"http://academic.oup.com/toxsci/article-pdf/144/1/65/16688123/kfu267.pdf"}],"createdAt":"2015-01-31","modifiedAt":"2017-08-23","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Cyclin-Dependent%20Kinase%20Inhibitor%20p21","dc:title":"Cyclin-Dependent Kinase Inhibitor p21"},{"@id":"https://cir.nii.ac.jp/all?q=DNA,%20Bacterial","dc:title":"DNA, Bacterial"},{"@id":"https://cir.nii.ac.jp/all?q=Male","dc:title":"Male"},{"@id":"https://cir.nii.ac.jp/all?q=Blotting,%20Western","dc:title":"Blotting, Western"},{"@id":"https://cir.nii.ac.jp/all?q=Apoptosis","dc:title":"Apoptosis"},{"@id":"https://cir.nii.ac.jp/all?q=Enzyme-Linked%20Immunosorbent%20Assay","dc:title":"Enzyme-Linked Immunosorbent Assay"},{"@id":"https://cir.nii.ac.jp/all?q=Kidney","dc:title":"Kidney"},{"@id":"https://cir.nii.ac.jp/all?q=Real-Time%20Polymerase%20Chain%20Reaction","dc:title":"Real-Time Polymerase Chain Reaction"},{"@id":"https://cir.nii.ac.jp/all?q=Histones","dc:title":"Histones"},{"@id":"https://cir.nii.ac.jp/all?q=Escherichia%20coli","dc:title":"Escherichia coli"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=DNA%20Breaks,%20Double-Stranded","dc:title":"DNA Breaks, Double-Stranded"},{"@id":"https://cir.nii.ac.jp/all?q=Oligonucleotide%20Array%20Sequence%20Analysis","dc:title":"Oligonucleotide Array Sequence Analysis"},{"@id":"https://cir.nii.ac.jp/all?q=Mice,%20Knockout","dc:title":"Mice, Knockout"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Expression%20Profiling","dc:title":"Gene Expression Profiling"},{"@id":"https://cir.nii.ac.jp/all?q=G1%20Phase%20Cell%20Cycle%20Checkpoints","dc:title":"G1 Phase Cell Cycle Checkpoints"},{"@id":"https://cir.nii.ac.jp/all?q=Immunohistochemistry","dc:title":"Immunohistochemistry"},{"@id":"https://cir.nii.ac.jp/all?q=Ochratoxins","dc:title":"Ochratoxins"},{"@id":"https://cir.nii.ac.jp/all?q=Kidney%20Neoplasms","dc:title":"Kidney Neoplasms"},{"@id":"https://cir.nii.ac.jp/all?q=Mice,%20Inbred%20C57BL","dc:title":"Mice, Inbred C57BL"},{"@id":"https://cir.nii.ac.jp/all?q=Disease%20Models,%20Animal","dc:title":"Disease Models, Animal"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Expression%20Regulation","dc:title":"Gene Expression Regulation"},{"@id":"https://cir.nii.ac.jp/all?q=Mutation","dc:title":"Mutation"},{"@id":"https://cir.nii.ac.jp/all?q=Comet%20Assay","dc:title":"Comet Assay"},{"@id":"https://cir.nii.ac.jp/all?q=Tumor%20Suppressor%20Protein%20p53","dc:title":"Tumor Suppressor Protein p53"},{"@id":"https://cir.nii.ac.jp/all?q=Signal%20Transduction","dc:title":"Signal Transduction"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000782240404992","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"25281027"},{"@type":"JGN","@value":"JP25281027"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25281027/"}],"notation":[{"@language":"ja","@value":"遺伝毒性物質の経世代的影響の定量的評価法に関する研究"},{"@language":"en","@value":"Studies on quantitative evaluation of inherited germline mutations"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360011144029894528","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"p53 in recombination and repair"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011146374608512","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"DNA damage-triggered apoptosis: critical role of DNA repair, double-strand breaks, cell proliferation and signaling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285709643125760","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Ochratoxin A induces DNA double-strand breaks and large deletion mutations in the carcinogenic target site of gpt delta rats"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292621123064320","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Implication of p53 in base excision DNA repair: in vivo 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Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699993888000256","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Effects of p53 knockout on ochratoxin A-induced genotoxicity in p53-deficient gpt delta mice"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699994400936704","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Reduction in Antioxidant Defenses may Contribute to Ochratoxin A Toxicity and Carcinogenicity"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699994793737856","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mutant frequency in comparison to oxidative DNA damage induced by ochratoxin A in L5178Y<i>tk</i><sup>+/−</sup>(3.7.2C) mouse lymphoma cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699995312100736","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Detecting, 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Carcinogenicity"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825893839018752","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Processing of O<sup>6</sup>-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell cycles"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825894430890112","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"p53 regulation of DNA excision repair pathways"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825895901106688","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"BH3-only proteins in apoptosis and beyond: an overview"}]},{"@id":"https://cir.nii.ac.jp/crid/1363107368755784448","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Modulation of key regulators of mitosis linked to chromosomal instability is an early event in ochratoxin A carcinogenicity"}]},{"@id":"https://cir.nii.ac.jp/crid/1363107370410297472","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"harakiri, a novel regulator of cell death, encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-XL"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388843542664320","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Inhibition of cyclin-dependent kinases by p21."}]},{"@id":"https://cir.nii.ac.jp/crid/1363388844235660416","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Molecular nature of intrachromosomal deletions and base substitutions induced by environmental mutagens"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670318728148352","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Other transgenic mutation assays: A new transgenic mouse mutagenesis test system using Spi− and 6-thioguanine selections"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670319963003264","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The ups and downs of p53: understanding protein dynamics in single cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670321171113216","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Break-Induced Replication Is Highly Inaccurate"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951795727613568","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"DNA double-strand breaks: signaling, repair and the cancer connection"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951795961323776","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Mutagenicity of Ochratoxin A and Its Hydroquinone Metabolite in the SupF Gene of the Mutation Reporter Plasmid 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