Endothelin suppresses cell migration via the JNK signaling pathway in a manner dependent upon Src kinase, Rac1, and Cdc42

FEBS Letters

Itoh, Hiroshi¹  Okamoto, Miyuki¹  Kokubu, Hiroshi¹  Yamauchi, Junji¹  Hirasawa, Akira²  Sugawara, Yo¹  Tsujimoto, Gozoh²  Nishii, Hiroko¹  Miyamoto, Yuki¹ 

[1] Department of Cell Biology, Graduate School of Biological Science, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0101, Japan;Department of Molecular Cell Pharmacology, National Center for Child Health and Development, Research Institute, 3-35-31 Taishido, Setagaya, Tokyo 154-8509, Japan

关键词: Cell motility;    Endothelin;    Src kinase;    Rac1;    Cdc42;    c-Jun N-terminal kinase;   

DOI  :  10.1016/S0014-5793(02)03231-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Cell migration is a complex phenomenon that is stimulated by chemoattractive factors such as chemokines, a family of ligands for G protein-coupled receptors (GPCRs). In contrast, factors that suppress cell migration, and the mechanism of their action, remain largely unknown. In this study, we show that endothelin, a GPCR ligand, inhibits cell motility in a manner dependent upon signaling through the c-Jun N-terminal kinase (JNK) pathway. We further demonstrate that this effect is dependent upon Src kinase and small GTPases Rac1 and Cdc42. These findings provide new insight into GPCR-mediated regulation of cell migration.

【 授权许可】

Unknown