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<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)
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| Item type | 紀要論文(ELS) / Departmental Bulletin Paper(ELS)(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2002-06-30 | |||||
| タイトル | ||||||
| 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 | |||||
| 言語 | ja | |||||
| タイトル | ||||||
| タイトル | <ORIGINAL REPORT>Phospatidylinositol 3-kinase regulates formation of invadopodia, promoting invasion in oral squamous cell carcinoma cells | |||||
| 言語 | en | |||||
| 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 |
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| 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 |
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木下, 隆二, 奥村, 一彦, 中村, 公則, 金澤, 正昭, 2002, <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: 25–42 p.
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