The mitogen-activated protein kinase p38-2 is necessary for the inhibition of N-type calcium current by bradykinin

Malgorzata A. Wilk-Blaszczak, Bernd Stein, Shuichan Xu, Miguel S. Barbosa, Melanie H. Cobb, Francesco Belardetti

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)112-118
Number of pages7
JournalJournal of Neuroscience
Volume18
Issue number1
DOIs
StatePublished - 1998

Keywords

  • Bradykinin
  • Calcium channels
  • G
  • G-protein
  • MAPK
  • NG108-15
  • Neuroblastoma x glioma
  • p38

ASJC Scopus subject areas

  • Neuroscience(all)

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