| タイトル |
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en
Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.
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| 作成者 |
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| アクセス権 |
open access |
| 主題 |
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MeSH
en
Animals
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MeSH
en
Cell Adhesion/physiology
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MeSH
en
Cells, Cultured
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MeSH
en
Extracellular Matrix Proteins/metabolism
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MeSH
en
Fibroblasts/metabolism
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MeSH
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Focal Adhesion Protein-Tyrosine Kinases/metabolism
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MeSH
en
Mice
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MeSH
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Phosphorylation
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MeSH
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Signal Transduction
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MeSH
en
Tenascin/metabolism
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MeSH
en
p38 Mitogen-Activated Protein Kinases/metabolism
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NDC
499
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| 内容注記 |
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Abstract
en
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.
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| 出版者 |
en
The Pharmaceutical Society of Japan
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| 日付 |
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| 言語 |
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| 資源タイプ |
journal article |
| 出版タイプ |
VoR |
| 資源識別子 |
HDL
http://hdl.handle.net/2115/53700
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| 関連 |
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isIdenticalTo
DOI
https://doi.org/10.1248/bpb.32.1795
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PMID
19801846
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| 収録誌情報 |
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en
Biological & pharmaceutical bulletin
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巻32
号10
開始ページ1795
終了ページ1799
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| ファイル |
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| コンテンツ更新日時 |
2023-07-26 |
