{"created":"2023-07-27T06:50:20.041109+00:00","id":43073,"links":{},"metadata":{"_buckets":{"deposit":"b14bd247-7e36-4b5c-8e86-e084a00b5f68"},"_deposit":{"created_by":18,"id":"43073","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"43073"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00043073","sets":["2812:2813:2819"]},"author_link":["69287","69288"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016-04-10","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"5p.","bibliographicVolumeNumber":"2012-04-01 – 2015-03-31","bibliographic_titles":[{"bibliographic_title":"平成26(2014)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2014 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"自律神経機能障害を持つ患者の中には、神経型アセチルコリン受容体（nAChRα3サブユニット）に対して自己抗体を持つ患者が存在する。我々はnAChRα3およびβ4サブユニットの過剰発現細胞を用い、患者血清とモノクローナル抗体の影響を調べた。患者血清を培養液に添加すると、細胞表面上のnAChR（α3β4）が細胞質内に取り込まれた。また、抗α3抗体はα3β4過剰発現細胞のα3サブユニット発現量を減少させ、細胞内Ca2+濃度上昇を抑えることがわかった。4℃で処理すると、細胞表面上α3サブユニットの減少はおこらなかったことより、エンドサイトーシスによる変化であることが示された。","subitem_description_type":"Abstract"},{"subitem_description":"There are patients with autoantibodies for neuronal acetylcholine receptor (nAChR alpha 3 subunit) with autonomic nervous system dysfunction. We used excessive expression cells of nAChR (alpha-3 and beta-4), and investigated the effects of patient’s serum and monoclonal anti-alpha-3 antibodies. Patient serum containing medium induced internalization of nAChR (alpha-3 and beta-4) into the cytoplasm. Monoclonal anti-alpha-3 antibodies decreased the expression of alpha-3 subunit and reduced the concentration of Ca2+ in cytoplasm. Processing at 4 °C revealed no decrease of alpha-3 subunit on the surface, that indicated endocytosis had a role in the process of decrease of alpha-3 subunits on the cell surface.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:24591253, 研究期間(年度):2012-04-01 – 2015-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「神経型アセチルコリン受容体を標的とした自己免疫性神経疾患」課題番号24591253\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所））\n（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-24591253/24591253seika/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学保健管理センター","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00049420","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=10272981"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=10272981","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24591253/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24591253/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-24591253/24591253seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-24591253/24591253seika/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-12-21"}],"displaytype":"detail","filename":"ME-PR-YOSHIKAWA-H-kaken 2016-5p.pdf","filesize":[{"value":"493.1 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-YOSHIKAWA-H-kaken 2016-5p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/43073/files/ME-PR-YOSHIKAWA-H-kaken 2016-5p.pdf"},"version_id":"8bf8962a-c148-47ce-995f-bfa72a90ec85"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"神経型アセチルコリン受容体を標的とした自己免疫性神経疾患","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"神経型アセチルコリン受容体を標的とした自己免疫性神経疾患"},{"subitem_title":"Autoimmune neurological diseases targeting neuronal acetylcholine receptor","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2819"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-12-22"},"publish_date":"2017-12-22","publish_status":"0","recid":"43073","relation_version_is_last":true,"title":["神経型アセチルコリン受容体を標的とした自己免疫性神経疾患"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T10:45:13.123531+00:00"}