{"created":"2023-07-27T06:55:04.222364+00:00","id":50731,"links":{},"metadata":{"_buckets":{"deposit":"f96896a2-1b88-4403-80c8-cb47d329b11c"},"_deposit":{"created_by":18,"id":"50731","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"50731"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00050731","sets":["2812:2813:2815"]},"author_link":["91861","91862"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2019-05-20","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"5p.","bibliographicVolumeNumber":"2017-04-01 – 2019-03-31","bibliographic_titles":[{"bibliographic_title":"平成30(2018)年度 科学研究費補助金 若手研究(B) 研究成果報告書"},{"bibliographic_title":"2018 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":"非アルコール性脂肪性肝炎(NASH)の病因はまだ不明であり、肝細胞癌(HCC)の発症予防は確立されていない。申請者は、ペレチノインがマウスの肝組織においてオートファジーを誘導することを見出した。NASH病態進行に伴い肝組織内のAtg16L1の発現の減少がみられた。HepG2細胞におけるAtg16L1の過剰発現は、パルミチン酸誘発NFκB活性化およびIL6 / STAT3活性化を阻害した。我々は、Atg16L1がIL6受容体であるGp130の脱リン酸化を誘導することを明らかにした。","subitem_description_type":"Abstract"},{"subitem_description":"The pathogenesis of non-alcoholic steatohepatitis (NASH) is still unclear and the prevention of the development of hepatocellular carcinoma (HCC) has not been established. We found that peretinoin induced autophagy in the liver of mice, which was characterized by the increased co-localized expression of LC3B-II and Lamp2, and increased autophagosome formation and autophagy flux in the liver. Especially, Atg16L1 was repressed at both the mRNA and protein level. Decreased Atg16L1 mRNA expression was also found in the liver of patients with NASH according to disease progression. Interestingly, Atg16L1 overexpression in HepG2 cells inhibited palmitate-induced NF-kB activation and IL6/ STAT3 activation. We showed that Atg16L1 induced the de-phosphorylation of Gp130, a receptor subunit of interleukin-6 family cytokines, which subsequently repressed phosphorylated STAT3 (Tyr705) levels, and this process might be independent of autophagy function.","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:17K15933, 研究期間(年度):2017-04-01 – 2019-03-31","subitem_description_type":"Other"},{"subitem_description":"出典:「慢性炎症を背景とした肝発がん・再発機序の解明」研究成果報告書 課題番号17K15933\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-17K15933/17K15933seika/)を加工して作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00057039","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学医薬保健学総合研究科"}]},"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=50788916"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=50788916","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K15933/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K15933/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K15933/17K15933seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K15933/17K15933seika/","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":"2020-04-16"}],"displaytype":"detail","filename":"ME-PR-OKADA-H-kaken 2019-5p.pdf","filesize":[{"value":"210.3 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-OKADA-H-kaken 2019-5p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/50731/files/ME-PR-OKADA-H-kaken 2019-5p.pdf"},"version_id":"0a733c89-7470-4657-9b69-6c678849a73e"}]},"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":"慢性炎症を背景とした肝発がん・再発機序の解明","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"慢性炎症を背景とした肝発がん・再発機序の解明"},{"subitem_title":"Analyzes the mechanism of liver tumorigenesis and recurrence through chronic inflammation","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2815"],"pubdate":{"attribute_name":"公開日","attribute_value":"2020-04-16"},"publish_date":"2020-04-16","publish_status":"0","recid":"50731","relation_version_is_last":true,"title":["慢性炎症を背景とした肝発がん・再発機序の解明"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:40:36.165823+00:00"}