Transactivation of the TPA-responsive element by the oncogenic c-erbB-2 protein is partly mediated by protein kinase C

Akiko Fujimoto, Sumio Kai, Tetsu Akiyama, Kumao Toyoshima, Kozo Kaibuchi, Yoshimi Takai, Tadashi Yamamoto

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The mutant c-erbB-2 gene encoding a protein with Glu instead of Val-659 in the transmembrane domain is able to transform NIH3T3 cells, while the wild type c-erbB-2 unless overexpressed does not. The mutant c-erbB-2 protein shows enhanced tyrosine kinase activity in vitro. Transient expression of this active c-erbB-2 stimulated the 12-O-tetradecanoylphorbol-13-acetate (TPA) response element, serum response element, and cyclic AMP response element. Particularly, stimulation of the TPA response element by active c-erbB-2 was prominent. In contrast, transient expression of wild type c-erbB-2 stimulated none of these elements. Transactivation of the TPA response element was also observed in a cell line that stably expresses active c-erbB-2. The active c-erbB-2-induced transactivation of the TPA response element was partially prevented either by down-regulation of protein kinase C or by the protein kinase C inhibitor H7. These results indicate that protein kinase C is partly involved in oncogenic signalling of the active c-erbB-2 protein that leads to Jun Fos-mediated transcriptional activation in nuclei.

Original languageEnglish
Pages (from-to)724-732
Number of pages9
JournalBiochemical and Biophysical Research Communications
Volume178
Issue number2
DOIs
Publication statusPublished - 31-07-1991

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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