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Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.
| Title: | Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation. |
| Authors: | Fujie, Shinpei Browse this author | | Maita, Hiroshi Browse this author →KAKEN DB | | Ariga, Hiroyoshi Browse this author →KAKEN DB | | Matsumoto, Ken-ichi Browse this author |
| Issue Date: | Oct-2009 |
| Publisher: | The Pharmaceutical Society of Japan |
| Journal Title: | Biological & pharmaceutical bulletin |
| Volume: | 32 |
| Issue: | 10 |
| Start Page: | 1795 |
| End Page: | 1799 |
| Publisher DOI: | 10.1248/bpb.32.1795 |
| PMID: | 19801846 |
| Abstract: | Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In this study, we investigated the adhesive properties of TNX and the signaling pathway to be induced to mouse fibroblast L cells on TNX substrate. Approximately 45% of evaluable cells used in the cell adhesion assay were attached to purified TNX but did not spread and were rounded on TNX. The remaining 55% of cells were detached from the TNX substrate and were floating in the conditioned medium. In rounded cells on TNX, phosphorylation of focal adhesion kinase (FAK) was diminished compared with that in cells on control phosphate buffered saline (PBS). To better understand the pathways that lead to the detachment of cells on the TNX substrate, we examined phosphorylation of p38 mitogen-activated protein (MAP) kinase. Phosphorylation of p38 MAP kinase was observed in the rounded cells on TNX in a dose-dependent manner, and the maximum effect was observed at 30 min on TNX. Inhibition of p38 MAP kinase alpha expression by RNA interference partially suppressed the TNX-induced cell detachment. These results suggest that the p38 MAP kinase is a major mediator of TNX-induced cell detachment. |
| Type: | article |
| URI: | http://hdl.handle.net/2115/53700 |
| Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 有賀 寛芳
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