{"_buckets": {"deposit": "054ee6c0-2e86-4289-832e-bc8de23824d3"}, "_deposit": {"created_by": 3, "id": "27370", "owners": [3], "pid": {"revision_id": 0, "type": "depid", "value": "27370"}, "status": "published"}, "_oai": {"id": "oai:kanazawa-u.repo.nii.ac.jp:00027370", "sets": ["1779"]}, "author_link": ["47477", "47471", "536", "47475", "47472", "47476", "47478", "47474", "74", "47473"], "item_4_biblio_info_8": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2007-04-21", "bibliographicIssueDateType": "Issued"}, "bibliographicPageStart": "37", "bibliographicVolumeNumber": "8", "bibliographic_titles": [{"bibliographic_title": "BMC Molecular Biology"}]}]}, "item_4_creator_33": {"attribute_name": "著者別表示", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "小林, 昌彦"}], "nameIdentifiers": [{"nameIdentifier": "536", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "70285633", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=70285633"}, {"nameIdentifier": "70285633", "nameIdentifierScheme": "金沢大学研究者情報", "nameIdentifierURI": "http://ridb.kanazawa-u.ac.jp/public/detail.php?kaken=70285633"}, {"nameIdentifier": "70285633", "nameIdentifierScheme": "研究者番号", "nameIdentifierURI": "https://nrid.nii.ac.jp/nrid/1000070285633"}]}, {"creatorNames": [{"creatorName": "山本, 健一"}], "nameIdentifiers": [{"nameIdentifier": "74", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "60115285", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=60115285"}, {"nameIdentifier": "60115285", "nameIdentifierScheme": "研究者番号", "nameIdentifierURI": "https://nrid.nii.ac.jp/nrid/1000060115285"}]}]}, "item_4_description_21": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "Background Previous studies suggest that human RAD9 (hRad9), encoding a DNA damage checkpoint molecule, which is frequently amplified in epithelial tumor cells of breast, lung, head and neck cancer, participates in regulation of the tumor suppressor p53-dependent transactivation of pro-survival P21WAF1. This study examined the exact mechanism of the hRad9 function, especially through the phosphorylation of the C-terminus, in the transcription regulation of P21WAF1. Results The transfection of phosphorylation-defective hRAD9 mutants of C-terminus resulted in reduction of the p53-dependent P21WAF1 transactivation; the knockdown of total hRad9 elicited an increased P21WAF1 mRNA expression. Immunoprecipitation and a ChIP assay showed that hRad9 and p53 formed a complex and both were associated with two p53-consensus DNA-binding sequences in the 5\u0027 region of P21WAF1 gene. The association was reduced in the experiment of phosphorylation-defective hRAD9 mutants. Conclusion The present study indicates the direct involvement of hRad9 in the p53-dependent P21WAF1 transcriptional mechanism, presumably via the phosphorylation sites, and alterations of the hRad9 pathway might therefore contribute to the perturbation of checkpoint activation in cancer cells.", "subitem_description_type": "Abstract"}]}, "item_4_description_5": {"attribute_name": "提供者所属", "attribute_value_mlt": [{"subitem_description": "金沢大学がん研究所がん分子細胞制御", "subitem_description_type": "Other"}]}, "item_4_identifier_registration": {"attribute_name": "ID登録", "attribute_value_mlt": [{"subitem_identifier_reg_text": "10.24517/00027357", "subitem_identifier_reg_type": "JaLC"}]}, "item_4_publisher_17": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "BioMed Central"}]}, "item_4_relation_12": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_type": "isVersionOf", "subitem_relation_type_id": {"subitem_relation_type_id_text": "10.1186/1471-2199-8-37", 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