{"created":"2023-05-15T09:57:30.158393+00:00","id":1321,"links":{},"metadata":{"_buckets":{"deposit":"60b21a53-f49f-480a-84f7-54649fd1d58b"},"_deposit":{"created_by":5,"id":"1321","owner":"5","owners":[5],"pid":{"revision_id":0,"type":"depid","value":"1321"},"status":"published"},"_oai":{"id":"oai:miyazaki-u.repo.nii.ac.jp:00001321","sets":["72","72:30"]},"author_link":["7812","7813","9591","7815","7816"],"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2009-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"e4152","bibliographicPageStart":"e4152","bibliographicVolumeNumber":"4","bibliographic_titles":[{"bibliographic_title":"PLoS ONE","bibliographic_titleLang":"en"}]}]},"item_10001_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins （RPs） play important roles in the\nformation of a functional ribosome. L11 was recently shown to regulate p53 activity through a direct binding with MDM2\nand abrogating the MDM2-induced p53 degradation in response to ribosomal stress. However, the studies were performed\nin cell lines and the significance of this tumor suppressor function of L11 has yet to be explored in animal models. To\ninvestigate the effects of the deletion of L11 and its physiological relevance to p53 activity, we knocked down the rpl11\ngene in zebrafish and analyzed the p53 response. Contrary to the cell line-based results, our data indicate that an L11\ndeficiency in a model organism activates the p53 pathway. The L11-deficient embryos （morphants） displayed\ndevelopmental abnormalities primarily in the brain, leading to embryonic lethality within 6–7 days post fertilization.\nExtensive apoptosis was observed in the head region of the morphants, thus correlating the morphological defects with\napparent cell death. A decrease in total abundance of genes involved in neural patterning of the brain was observed in the\nmorphants, suggesting a reduction in neural progenitor cells. Upregulation of the genes involved in the p53 pathway were\nobserved in the morphants. Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in\nthe morphants. These results suggest that ribosomal dysfunction due to the loss of L11 activates a p53-dependent\ncheckpoint response to prevent improper embryonic development.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10001_publisher_8":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Public Library of Science (PLoS)","subitem_publisher_language":"en"}]},"item_10001_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"19326203","subitem_source_identifier_type":"ISSN"}]},"item_10001_version_type_20":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"剣持, 直哉","creatorNameLang":"ja"},{"creatorName":"ケンモチ, ナオヤ","creatorNameLang":"ja-Kana"},{"creatorName":"Kenmochi, Naoya","creatorNameLang":"en"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Chakraborty, Anirban","creatorNameLang":"en"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Uechi, Tamayo","creatorNameLang":"en"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"Higa, Sayomi","creatorNameLang":"en"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Torihara, Hidetsugu","creatorNameLang":"en"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-06-21"}],"displaytype":"detail","filename":"kenmochi_plosone_2009.pdf","filesize":[{"value":"370.2 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"kenmochi  plosone 2009.pdf","url":"https://miyazaki-u.repo.nii.ac.jp/record/1321/files/kenmochi_plosone_2009.pdf"},"version_id":"7d8c7e63-eece-4b8f-9316-d3fe7b2715ae"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"protein l 11, protein p53, ribosome protein, brain development, developmental disorder, embryo development, protein depletion, protein function","subitem_subject_language":"en","subitem_subject_scheme":"Other"}]},"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":"Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response","subitem_title_language":"en"}]},"item_type_id":"10001","owner":"5","path":["72","30"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2009-03-02"},"publish_date":"2009-03-02","publish_status":"0","recid":"1321","relation_version_is_last":true,"title":["Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response"],"weko_creator_id":"5","weko_shared_id":2},"updated":"2024-01-30T04:24:58.968891+00:00"}