Modulation of α(1B)-adrenoceptor expression by agonist and protein kinase inhibitors

Kristin S. Bird, Jodi L. Anderson, Myron L. Toews

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

The agonist-induced up-regulation of α(1B)-adrenoceptors in clone H99 of transfected Chinese hamster ovary cells that we reported previously (Zhu et al., 1996) was further investigated. Studies with a larger number of clones revealed that the up-regulation observed in H99) cells is atypical and that most other clones exhibit down-regulation under the same conditions. The role of protein kinases in the up-regulation of α(1B)-adrenoceptors in clone H99 was further investigated. Surprisingly, the protein kinase inhibitor staurosporine induced a similar up-regulation. Neither the selective protein kinase C inhibitor GF109203X nor the activator phorbol 12-myristate, 13-acetate altered receptor expression. The tyrosine kinase inhibitors genistein and its weaker analog daidzein did not induce up-regulation but blocked the up-regulation induced by epinephrine and by staurosporine. Up-regulation was blocked by the protein synthesis inhibitor cycloheximide. These studies suggest multiple mechanisms by which different protein kinases can modulate the expression of transfected α(1B)-adrenoceptors.

Original languageEnglish (US)
Pages (from-to)267-275
Number of pages9
JournalEuropean Journal of Pharmacology
Volume340
Issue number2-3
DOIs
StatePublished - Dec 11 1997

Keywords

  • Genistein
  • Protein kinase
  • Receptor down-regulation
  • Receptor up-regulation
  • Staurosporine
  • α(1B)-Adrenoceptor

ASJC Scopus subject areas

  • Pharmacology

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