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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.
Naraba, H; Ueno, A; Kosugi, Y; Yoshimura, M; Murakami, M; Kudo, I; Oh-ishi, S.
Affiliation
  • Naraba H; Department of Pharmacology, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.
FEBS Lett ; 435(1): 96-100, 1998 Sep 11.
Article in En | MEDLINE | ID: mdl-9755866
ABSTRACT
In response to bradykinin, phosphorylated MAP kinases (ERK-1 and ERK-2) were abundantly increased in HEK 293 cells, which overexpress the rat B2 kinin receptor. In a similar way des-Arg9-bradykinin stimulation of B1 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 B1 and B2 kinin receptors mediating the MAP kinase signaling pathway to activate AP-1.
Subject(s)
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Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / Receptors, Bradykinin / Calcium-Calmodulin-Dependent Protein Kinases / Transcription Factor AP-1 Type of study: Etiology_studies Limits: Animals / Humans Language: En Journal: FEBS Lett Year: 1998 Document type: Article Affiliation country: Japón
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Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / Receptors, Bradykinin / Calcium-Calmodulin-Dependent Protein Kinases / Transcription Factor AP-1 Type of study: Etiology_studies Limits: Animals / Humans Language: En Journal: FEBS Lett Year: 1998 Document type: Article Affiliation country: Japón