{"created":"2021-03-01T06:17:31.176603+00:00","id":966,"links":{},"metadata":{"_buckets":{"deposit":"53bd8df2-5830-4b9f-b779-4df5800dddf0"},"_deposit":{"id":"966","owners":[],"pid":{"revision_id":0,"type":"depid","value":"966"},"status":"published"},"_oai":{"id":"oai:repository.dl.itc.u-tokyo.ac.jp:00000966","sets":["20:229:230","9:10:11"]},"item_2_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016-05-14","bibliographicIssueDateType":"Issued"},"bibliographic_titles":[{"bibliographic_title":"Human Molecular Genetics Online Edition"}]}]},"item_2_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"BIN1 is a genetic risk factor of late-onset Alzheimer disease (AD), which was identified in multiple genome-wide association studies. BIN1 is a member of the amphiphysin family of proteins, and contains N-terminal Bin-Amphiphysin-Rvs and C-terminal Src homology 3 domains. BIN1 is widely expressed in the mouse and human brains, and has been reported to function in the endocytosis and the endosomal sorting of membrane proteins. BACE1 is a type 1 transmembrane aspartyl protease expressed predominantly in neurons of the brain and responsible for the production of amyloid-β peptide (Aβ). Here we report that the depletion of BIN1 increases cellular BACE1 levels through impaired endosomal trafficking and reduces BACE1 lysosomal degradation, resulting in increased Aβ production. Our findings provide a mechanistic role of BIN1 in the pathogenesis of AD as a novel genetic regulator of BACE1 levels and Aβ production.","subitem_description_type":"Abstract"}]},"item_2_description_6":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"UTokyo Research掲載「細胞内の輸送の乱れがアルツハイマー病を引き起こす」 URI: http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/disruption-of-intracellular-transport-shown-to-trigger-alzheimers-disease.html","subitem_description_type":"Other"},{"subitem_description":"UTokyo Research \"Disruption of intracellular transport shown to trigger Alzheimer’s disease\" URI: http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/disruption-of-intracellular-transport-shown-to-trigger-alzheimers-disease.html","subitem_description_type":"Other"}]},"item_2_publisher_20":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Oxford University Press"}]},"item_2_relation_11":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"info:doi/10.1093/hmg/ddw146","subitem_relation_type_select":"DOI"}}]},"item_2_relation_25":{"attribute_name":"関係URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/disruption-of-intracellular-transport-shown-to-trigger-alzheimers-disease.html","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/disruption-of-intracellular-transport-shown-to-trigger-alzheimers-disease.html","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://hmg.oxfordjournals.org/content/early/2016/05/30/hmg.ddw146.abstract","subitem_relation_type_select":"URI"}}]},"item_2_rights_12":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"© The Author (2016). Published by Oxford University Press on behalf of the Human Molecular Genetics. All rights reserved."}]},"item_2_select_14":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_select_item":"author"}]},"item_2_source_id_10":{"attribute_name":"書誌レコードID","attribute_value_mlt":[{"subitem_source_identifier":"AA12095462","subitem_source_identifier_type":"NCID"}]},"item_2_source_id_8":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1460-2083","subitem_source_identifier_type":"ISSN"}]},"item_2_text_4":{"attribute_name":"著者所属","attribute_value_mlt":[{"subitem_text_value":"Laboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences"},{"subitem_text_value":"Department of Neurology, Graduate School of Medicine, The University of Tokyo"},{"subitem_text_value":"Lankenau Institute for Medical Research"},{"subitem_text_value":"Laboratory of Natural Products Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya University"},{"subitem_text_value":"Department of Neuropathology, Graduate School of Medicine, The University of Tokyo"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Miyagawa, Toji"}],"nameIdentifiers":[{"nameIdentifier":"3969","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Ebinuma, Ihori"}],"nameIdentifiers":[{"nameIdentifier":"3970","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Morohashi, Yuichi"}],"nameIdentifiers":[{"nameIdentifier":"3971","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Hori, Yukiko"}],"nameIdentifiers":[{"nameIdentifier":"3972","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Chang, Mee Young"}],"nameIdentifiers":[{"nameIdentifier":"3973","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Hattori, Haruhiko"}],"nameIdentifiers":[{"nameIdentifier":"3974","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Maehara, Tomoaki"}],"nameIdentifiers":[{"nameIdentifier":"3975","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Yokoshima, Satoshi"}],"nameIdentifiers":[{"nameIdentifier":"3976","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Fukuyama, Tohru"}],"nameIdentifiers":[{"nameIdentifier":"3977","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Tsuji, Shoji"}],"nameIdentifiers":[{"nameIdentifier":"3978","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Iwatsubo, Takeshi"}],"nameIdentifiers":[{"nameIdentifier":"3979","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Prendergast, George C."}],"nameIdentifiers":[{"nameIdentifier":"3980","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Tomita, Taisuke"}],"nameIdentifiers":[{"nameIdentifier":"3981","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-05-30"}],"displaytype":"detail","filename":"10.1093_hmg_ddw146.pdf","filesize":[{"value":"2.3 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"10.1093_hmg_ddw146.pdf","url":"https://repository.dl.itc.u-tokyo.ac.jp/record/966/files/10.1093_hmg_ddw146.pdf"},"version_id":"4ef9f67f-1cfd-4b59-973a-6ee368c39953"}]},"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":"BIN1 regulates BACE1 intracellular trafficking and amyloid-β production","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"BIN1 regulates BACE1 intracellular trafficking and amyloid-β production"}]},"item_type_id":"2","owner":"1","path":["11","230"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-05-15"},"publish_date":"2017-05-15","publish_status":"0","recid":"966","relation_version_is_last":true,"title":["BIN1 regulates BACE1 intracellular trafficking and amyloid-β production"],"weko_creator_id":"1","weko_shared_id":null},"updated":"2022-12-19T03:42:13.109686+00:00"}