{"created":"2023-06-26T11:01:08.884862+00:00","id":1771,"links":{},"metadata":{"_buckets":{"deposit":"879143ee-af51-4f98-a546-4daaa7270a87"},"_deposit":{"created_by":30,"id":"1771","owners":[30],"pid":{"revision_id":0,"type":"depid","value":"1771"},"status":"published"},"_oai":{"id":"oai:oist.repo.nii.ac.jp:00001771","sets":["6:67"]},"author_link":["10622","10623","10621","10624","10628","10625","10627","10626"],"item_10001_biblio_info_7":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2020-08-28","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageStart":"476","bibliographicVolumeNumber":"3","bibliographic_titles":[{},{"bibliographic_title":"Communications Biology","bibliographic_titleLang":"en"}]}]},"item_10001_creator_3":{"attribute_name":"Author","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Mostafa, Dina"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Yanagiya, Akiko"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Georgiadou, Eleni"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Wu, Yibo"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Stylianides, Theodoros"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Rutter, Guy A."}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Suzuki, Toru"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Yamamoto, Tadashi"}],"nameIdentifiers":[{}]}]},"item_10001_description_5":{"attribute_name":"Abstract","attribute_value_mlt":[{"subitem_description":"Pancreatic β-cells are responsible for production and secretion of insulin in response to increasing blood glucose levels. Defects in β-cell function lead to hyperglycemia and diabetes mellitus. Here, we show that CNOT3, a CCR4-NOT deadenylase complex subunit, is dysregulated in islets in diabetic db/db mice, and that it is essential for murine β cell maturation and identity. Mice with β cell-specific Cnot3 deletion (Cnot3βKO) exhibit impaired glucose tolerance, decreased β cell mass, and they gradually develop diabetes. Cnot3βKO islets display decreased expression of key regulators of β cell maturation and function. Moreover, they show an increase of progenitor cell markers, β cell-disallowed genes, and genes relevant to altered β cell function. Cnot3βKO islets exhibit altered deadenylation and increased mRNA stability, partly accounting for the increased expression of those genes. Together, these data reveal that CNOT3-mediated mRNA deadenylation and decay constitute previously unsuspected post-transcriptional mechanisms essential for β cell identity.","subitem_description_type":"Other"}]},"item_10001_publisher_8":{"attribute_name":"Publisher","attribute_value_mlt":[{"subitem_publisher":"Nature Research"}]},"item_10001_relation_13":{"attribute_name":"PubMedNo.","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"info:pmid/32859966","subitem_relation_type_select":"PMID"}}]},"item_10001_relation_14":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"info:doi/10.1038/s42003-020-01201-y","subitem_relation_type_select":"DOI"}}]},"item_10001_relation_17":{"attribute_name":"Related site","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://www.nature.com/articles/s42003-020-01201-y","subitem_relation_type_select":"URI"}}]},"item_10001_rights_15":{"attribute_name":"Rights","attribute_value_mlt":[{"subitem_rights":"© 2020 The Author(s)"}]},"item_10001_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"2399-3642","subitem_source_identifier_type":"ISSN"}]},"item_10001_version_type_20":{"attribute_name":"Author's flag","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-11-11"}],"displaytype":"detail","filename":"Mostafa-2020-Loss of beta-cell identity and di.pdf","filesize":[{"value":"2.6 MB"}],"format":"application/pdf","license_note":"Creative Commons Attribution 4.0 International(https://creativecommons.org/licenses/by/4.0/)","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"Mostafa-2020-Loss of beta-cell identity and di","url":"https://oist.repo.nii.ac.jp/record/1771/files/Mostafa-2020-Loss of beta-cell identity and di.pdf"},"version_id":"6866fe3f-17c0-46ea-ac59-c54b23c53609"}]},"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 β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation","subitem_title_language":"en"}]},"item_type_id":"10001","owner":"30","path":["67"],"pubdate":{"attribute_name":"公開日","attribute_value":"2020-11-11"},"publish_date":"2020-11-11","publish_status":"0","recid":"1771","relation_version_is_last":true,"title":["Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation"],"weko_creator_id":"30","weko_shared_id":30},"updated":"2023-06-26T11:43:10.779854+00:00"}