مورد إلكتروني

Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.

التفاصيل البيبلوغرافية
العنوان: Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.
بيانات النشر: The Pharmaceutical Society of Japan 2009-10
تفاصيل مُضافة: Fujie, Shinpei
Maita, Hiroshi
Ariga, Hiroyoshi
Matsumoto, Ken-ichi
نوع الوثيقة: Electronic Resource
مستخلص: 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.
مصطلحات الفهرس: Animals, Cell Adhesion/physiology, Cells, Cultured, Extracellular Matrix Proteins/metabolism, Fibroblasts/metabolism, Focal Adhesion Protein-Tyrosine Kinases/metabolism, Mice, Phosphorylation, Signal Transduction, Tenascin/metabolism, p38 Mitogen-Activated Protein Kinases/metabolism, 499, article
URL: http://hdl.handle.net/2115/53700Test
الإتاحة: Open access content. Open access content
ملاحظة: English
أرقام أخرى: YX@ oai:eprints.lib.hokudai.ac.jp:2115/53700
Biological & pharmaceutical bulletin, 32(10): 1795-1799
1198365882
المصدر المساهم: HOKKAIDO UNIV
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رقم الانضمام: edsoai.on1198365882
قاعدة البيانات: OAIster