WEKO3
アイテム
{"_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": ["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", "download_preview_message": "", "file_order": 0, "filename": "KJ00000095984.pdf", "filesize": [{"value": "1.8 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "mimetype": "application/pdf", "size": 1800000.0, "url": {"label": "\u003c原著\u003ePhosphatidylinositol 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": "\u003c原著\u003ePhosphatidylinositol 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": "\u003c原著\u003ePhosphatidylinositol 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": "\u003cORIGINAL REPORT\u003ePhospatidylinositol 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"], "permalink_uri": "https://hsuh.repo.nii.ac.jp/records/8712", "pubdate": {"attribute_name": "PubDate", "attribute_value": "2002-06-30"}, "publish_date": "2002-06-30", "publish_status": "0", "recid": "8712", "relation": {}, "relation_version_is_last": true, "title": ["\u003c原著\u003ePhosphatidylinositol 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_shared_id": -1}
<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
https://hsuh.repo.nii.ac.jp/records/8712
https://hsuh.repo.nii.ac.jp/records/871265d88917-6b6d-45b5-8d12-8147b84526ee
名前 / ファイル | ライセンス | アクション |
---|---|---|
<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 (1.8 MB)
|
|
Item type | 紀要論文(ELS) / Departmental Bulletin Paper(ELS)(1) | |||||
---|---|---|---|---|---|---|
公開日 | 2002-06-30 | |||||
タイトル | ||||||
言語 | ja | |||||
タイトル | <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 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | <ORIGINAL REPORT>Phospatidylinositol 3-kinase regulates formation of invadopodia, promoting invasion in oral squamous cell carcinoma cells | |||||
言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | phosphatdylinositol 3-kinase | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | oral squamous cell carcinoma cells | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | invadopodia | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | departmental bulletin paper | |||||
ページ属性 | ||||||
内容記述タイプ | Other | |||||
内容記述 | P(論文) | |||||
言語 | ja | |||||
著者名(日) |
木下, 隆二
× 木下, 隆二× 奥村, 一彦× 中村, 公則× 金澤, 正昭 |
|||||
著者所属(日) | ||||||
ja | ||||||
北海道医療大学歯学部口腔外科学第一講座 | ||||||
著者所属(英) | ||||||
en | ||||||
1st Deparment of oral and maxilofacial surgery, School of dentistry, Health Sciences University of Hokkaido | ||||||
抄録(英) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 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. | |||||
言語 | en | |||||
雑誌書誌ID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN0008135X | |||||
書誌情報 |
ja : 東日本歯学雑誌 巻 21, 号 1, p. 25-42, 発行日 2002-06-30 |