Agonist stimulation of B1 and B2 kinin receptors causes activation of the MAP kinase signaling pathway, resulting in the translocation of AP-1 in HEK 293 cells

被引:23
作者
Naraba, H
Ueno, A
Kosugi, Y
Yoshimura, M
Murakami, M
Kudo, I
Oh-Ishi, S
机构
[1] Kitasato Univ, Sch Pharmaceut Sci, Dept Pharmacol, Minato Ku, Tokyo 1088641, Japan
[2] Showa Univ, Sch Pharmaceut Sci, Dept Hlth Chem, Shinagawa Ku, Tokyo 1428555, Japan
关键词
Bradykinin; B-1 kinin receptor; activator protein-1; mitogen-activated protein kinase;
D O I
10.1016/S0014-5793(98)01045-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In response to bradykinin, phosphorylated MAP kinases (ERK-1 and ERK-2) were abundantly increased in HEK 293 cells, which overexpress the rat B-2 kinin receptor. In a similar may des-Arg(9)-bradykinin stimulation of B-1 kinin receptor-overexpressing HEK 293 cells caused activation of the same species of MAP kinase, Furthermore, nuclear translocation of transcription factor AP-1 was also found in the cells after stimulation with either agonist, PD98059, a MAP kinase kinase (MEK-1) inhibitor, blocked the agonist-induced AP-1 translocation as well as the phosphorylation of the MAP kinases, This communication provides the first evidence for both B-1 and B-2 kinin receptors mediating the MAP kinase signaling pathway to activate AP-1, (C) 1998 Federation of European Biochemical Societies.
引用
收藏
页码:96 / 100
页数:5
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