Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

Chuanshu Huang, Wei-Ya Ma, Zigang Dong

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

The exposure of mammalian cells to ultraviolet (u.v.) irradiation leads to activation of transcription factors, such as AP-1 and NFκB. It is postulated that the EGF receptor but not protein kinase C (PKC) is the major membrane mediator in UVC-induced signal transduction. We demonstrate here that the antisense oligonucleotides of PKCζ and the dominant negative mutant of PKCλ/ι as well as dominant negative PKCζ markedly blocked UVC-induced AP-1 activity. In contrast, UVC-induced AP-1 activity in cells devoid of the EGF receptor (B82), is not significantly different from that of the stable transfectants with a kinase-deficient EGF receptor (B82M721), or wild-type EGF receptor (B82L). This was found at all UVC irradiation doses and time courses studied, while high levels of EGF-induced AP-1 activity were observed in B82L cells but not in B82 cells. This evidence strongly suggests that atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in JB6 and B82 cells.

Original languageEnglish (US)
Pages (from-to)1945-1954
Number of pages10
JournalOncogene
Volume14
Issue number16
DOIs
StatePublished - 1997

Bibliographical note

Funding Information:
This work was supported by the Hormel Foundation. We thank Dr HHO Schmid and WH Anderson for critical reading, Dr GN Gill for providing us with the B82, B82L and B82M721 cell lines, Dr J Moscat and JS Gutkind for generous gifts of dominant negative mutant of Xenopus PKCl/i and rat PKCz, respectively, and Ms C Perleberg and Ms Jeanne A Ruble for secretarial assistance.

Keywords

  • AP-1
  • Epidermal growth factor receptor
  • Protein kinase C
  • Ultraviolet

Fingerprint

Dive into the research topics of 'Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells'. Together they form a unique fingerprint.

Cite this