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The Journal of Neuroscience, January 1, 1998, 18(1):112-118

The Mitogen-Activated Protein Kinase p38-2 Is Necessary for the Inhibition of N-Type Calcium Current by Bradykinin

Malgorzata A. Wilk-Blaszczak¹, Bernd Stein², Shuichan Xu¹, Miguel S. Barbosa², Melanie H. Cobb¹, and Francesco Belardetti¹

¹ Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas 75235, and ² Signal Pharmaceuticals, Inc., San Diego, California 92121

Calcium influx via voltage-dependent calcium channels (I_Ca,V) links depolarization of excitable cells to critical cellular processes, such as secretion, contraction, and gene transcription. Fast regulation of I_Ca,V (<1 sec) by G-protein-coupled receptors is a relatively well-defined mechanism, whereas slow (30-60 sec) actions of transmitters and hormones on the same current remain poorly understood. In NG108-15 cells, the kinetically slow inhibition of N-type I_Ca,V by bradykinin (BK) requires the sequential activation of two G-proteins, heterotrimeric G₁₃ and monomeric Rac1/Cdc42. We have now defined a role in this pathway for the relatively fast-acting p38 mitogen-activated protein kinase (MAPK). The slow inhibition of I_Ca,V by BK was suppressed specifically by SB203580, a compound that inhibits the p38 family of MAPKs. BK potently and selectively activated a newly discovered p38 family member, p38-2. These data provide the first evidence that a MAPK is involved in the regulation of I_Ca,V by a receptor-mediated process.

Key words: G-protein; calcium channels; bradykinin; p38; MAPK; neuroblastoma x glioma; NG108-15; G₁₃

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Copyright © 1998 Society for Neuroscience  0270-6474/98/181112-07$05.00/0

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