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Wortmannin inhibits the activation of MAP kinase following vasopressin V1 receptor stimulation
Author(s) -
Naoya Nishioka,
Syu-ichi Hirai,
Keiko Mizuno,
ShinIchi Osada,
Atsushi Suzuki,
Kenji Kosaka,
Shigeo Ohno
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01382-2
Subject(s) - wortmannin , vasopressin , kinase , chemistry , mitogen activated protein kinase , protein kinase c , receptor antagonist , vasopressin receptor , microbiology and biotechnology , antagonist , receptor , endocrinology , medicine , biology , biochemistry , phosphatidylinositol
Treatment of rat 3Y1 fibroblasts with vasopressin (AVP) results in a transient activation of MAP kinase as potent as with EGF and serum. An antagonist of vasopressin receptor V1, but not an antagonist of V2, inhibited the AVP‐induced activation of MAP kinases, indicating that AVP activates MAP kinases through V1 receptor. Prolonged TPA treatment of cells resulted in partial MAP kinase activation, indicating the presence of PKC‐independent pathway. The pathway was inhibited by wortmannin, an inhibitor of PI3‐kinase. The results suggest that wortmannin‐sensitive molecules such as PI3‐kinase, are involved in the V1 receptor‐mediated activation of the MAP kinase pathway independent of TPA‐sensitive PKC.