{"created":"2023-05-15T11:32:18.724026+00:00","id":8712,"links":{},"metadata":{"_buckets":{"deposit":"5fffab14-ce52-46c7-9cc8-ef7b4d693745"},"_deposit":{"created_by":17,"id":"8712","owners":[17],"pid":{"revision_id":0,"type":"depid","value":"8712"},"status":"published"},"_oai":{"id":"oai:hsuh.repo.nii.ac.jp:00008712","sets":["89:570"]},"author_link":["26327","37283","37284","37285"],"item_2_biblio_info_14":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2002-06-30","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"42","bibliographicPageStart":"25","bibliographicVolumeNumber":"21","bibliographic_titles":[{"bibliographic_title":"東日本歯学雑誌","bibliographic_titleLang":"ja"}]}]},"item_2_creator_6":{"attribute_name":"著者名(日)","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"木下, 隆二","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"26327","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"奥村, 一彦","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"37283","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"中村, 公則","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"37284","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"金澤, 正昭","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"37285","nameIdentifierScheme":"WEKO"}]}]},"item_2_description_1":{"attribute_name":"ページ属性","attribute_value_mlt":[{"subitem_description":"P(論文)","subitem_description_language":"ja","subitem_description_type":"Other"}]},"item_2_description_12":{"attribute_name":"抄録(英)","attribute_value_mlt":[{"subitem_description":"Aggressively invasive human oral squamous cell carcinoma cells as SAS-H1 have the ability to extend membrane protrusions, invadopodia, into the extracellular matrix . These structures are associated with sites of active matrix degradation. The amount of membrane protrusions has been shown to correlate directly with the invasive potential. Immunofluorescent staining using mAb phospatidylinositol 3-kinase (PI3-K) p85α shows that the P13-K p85 regulatory subunit is predominantly associated with invadopodia, coreresponding to the areas where fibronectin / gelatin degradation occurs. We demonstrate that PI3-K inhibitors (wortmannin and LY294002) blocks local extracellular matrix degradation and formation of invadopodia. The SAS-H1 cells were sheared from the surface of a gelatin matrix to isolate invadopodia. The PI3-K p85 regulatory subunit and PI3-K p110α catalytic subunit were co -immunoprecipitated as a complex from invadopodia by Western blotting. PI3-K activity was higher in the invadopodia fraction than in the cell body fraction. These findings suggest that PI3-K has a direct role in the regulation of invadopodia activity.","subitem_description_language":"en","subitem_description_type":"Other"}]},"item_2_source_id_13":{"attribute_name":"雑誌書誌ID","attribute_value_mlt":[{"subitem_source_identifier":"AN0008135X","subitem_source_identifier_type":"NCID"}]},"item_2_text_10":{"attribute_name":"著者所属(英)","attribute_value_mlt":[{"subitem_text_language":"en","subitem_text_value":"1st Deparment of oral and maxilofacial surgery, School of dentistry, Health Sciences University of Hokkaido"}]},"item_2_text_9":{"attribute_name":"著者所属(日)","attribute_value_mlt":[{"subitem_text_language":"ja","subitem_text_value":"北海道医療大学歯学部口腔外科学第一講座"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2002-06-30"}],"displaytype":"detail","filename":"KJ00000095984.pdf","filesize":[{"value":"1.8 MB"}],"format":"application/pdf","mimetype":"application/pdf","url":{"label":"<原著>Phosphatidylinositol 3-kinase(PI3-K)は口腔扁平上皮癌細胞の浸潤突起形成を制御している","objectType":"fulltext","url":"https://hsuh.repo.nii.ac.jp/record/8712/files/KJ00000095984.pdf"},"version_id":"f2c32d6c-6ff9-418a-929d-1421f1a12229"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"phosphatdylinositol 3-kinase","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"oral squamous cell carcinoma cells","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"invadopodia","subitem_subject_language":"en","subitem_subject_scheme":"Other"}]},"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":"departmental bulletin paper","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"<原著>Phosphatidylinositol 3-kinase(PI3-K)は口腔扁平上皮癌細胞の浸潤突起形成を制御している","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"<原著>Phosphatidylinositol 3-kinase(PI3-K)は口腔扁平上皮癌細胞の浸潤突起形成を制御している","subitem_title_language":"ja"},{"subitem_title":"<ORIGINAL REPORT>Phospatidylinositol 3-kinase regulates formation of invadopodia, promoting invasion in oral squamous cell carcinoma cells","subitem_title_language":"en"}]},"item_type_id":"2","owner":"17","path":["570"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2002-06-30"},"publish_date":"2002-06-30","publish_status":"0","recid":"8712","relation_version_is_last":true,"title":["<原著>Phosphatidylinositol 3-kinase(PI3-K)は口腔扁平上皮癌細胞の浸潤突起形成を制御している"],"weko_creator_id":"17","weko_shared_id":-1},"updated":"2024-02-27T23:59:27.437417+00:00"}