@article{oai:hsuh.repo.nii.ac.jp:00008712,
 author = {木下, 隆二 and 奥村, 一彦 and 中村, 公則 and 金澤, 正昭},
 issue = {1},
 journal = {東日本歯学雑誌},
 month = {Jun},
 note = {P(論文), 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.},
 pages = {25--42},
 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},
 volume = {21},
 year = {2002}
}