{"created":"2023-05-15T14:35:10.480976+00:00","id":45365,"links":{},"metadata":{"_buckets":{"deposit":"f369e1a6-7933-4634-a1f7-e93f00f1b295"},"_deposit":{"created_by":1,"id":"45365","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"45365"},"status":"published"},"_oai":{"id":"oai:repo.qst.go.jp:00045365","sets":["1"]},"author_link":["450645","450650","450649","450651","450647","450653","450648","450646","450655","450654","450652"],"item_8_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2008-08","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"2","bibliographicPageEnd":"223","bibliographicPageStart":"216","bibliographicVolumeNumber":"170","bibliographic_titles":[{"bibliographic_title":"Radiation Research"}]}]},"item_8_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"With the goal of understanding the role of non-homologous end-joining repair in the maintenance of genetic information at the tissue level, we studied mutations induced by radiation and subsequent repair of DNA double-strand breaks in Ku70 gene-deficient lacZ transgenic mice. The local mutation frequencies and types of mutations were analyzed on a lacZ gene that had been chromosomally integrated, which allowed us to monitor DNA sequence alterations within this 3.1-kbp region. The mutagenic process leading to the development of the most frequently observed small deletions in wild-type mice after exposure to 20 Gy of X rays was suppressed in Ku70 mice in the three tissues examined: spleen, liver and brain. Examination of DNA break rejoining and the phosphorylation of histone H2AX in Ku70-deficient and -proficient mice revealed that Ku70 deficiency decreased the frequency of DNA rejoining, suggesting that DNA rejoining is one of the causes of radiation-induced deletion mutations. Limited but statistically significant DNA rejoining was found in the liver and brain of Ku70-deficient mice 3.5 days after irradiation, showing the presence of a DNA double-strand break repair system other than non-homologous end joining. These data indicate a predominant role of non-homologous end joining in the production of radiation-induced mutations in vivo.","subitem_description_type":"Abstract"}]},"item_8_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0033-7587","subitem_source_identifier_type":"ISSN"}]},"item_access_right":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"metadata only access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_14cb"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Uehara, Yosihiko"}],"nameIdentifiers":[{"nameIdentifier":"450645","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Ikehata, Hironobu"}],"nameIdentifiers":[{"nameIdentifier":"450646","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Hirayama, Ryoichi"}],"nameIdentifiers":[{"nameIdentifier":"450647","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Furusawa, Yoshiya"}],"nameIdentifiers":[{"nameIdentifier":"450648","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Ando, Koichi"}],"nameIdentifiers":[{"nameIdentifier":"450649","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Ono, Tetsuya"}],"nameIdentifiers":[{"nameIdentifier":"450650","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"et.al"}],"nameIdentifiers":[{"nameIdentifier":"450651","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"上原 芳彦","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"450652","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"平山 亮一","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"450653","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"古澤 佳也","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"450654","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"安藤 興一","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"450655","nameIdentifierScheme":"WEKO"}]}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues"}]},"item_type_id":"8","owner":"1","path":["1"],"pubdate":{"attribute_name":"公開日","attribute_value":"2008-12-25"},"publish_date":"2008-12-25","publish_status":"0","recid":"45365","relation_version_is_last":true,"title":["Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues"],"weko_creator_id":"1","weko_shared_id":-1},"updated":"2023-05-16T00:04:35.083397+00:00"}