Ultraviolet B-induced activated protein-1 activation does not require epidermal growth factor receptor but is blocked by a dominant negative PKCλ/l

Chuanshu Huang, Wei-Ya Ma, Tim Bowden, Zigang Dong

Research output: Contribution to journalArticle

109 Scopus citations

Abstract

The exposure of mammalian cells to UV irradiation leads to the activation of transcription factors such as activated protein-1 (AP-1) and NFκB. It is postulated that epidermal growth factor (EGF) receptor, but not protein kinase C (PKC), is the major membrane mediator in UV-induced signal transduction. Since UVB is responsible for most of the carcinogenic effects of sun exposure, we investigated the role of EGF receptors and PKC in UVB- induced AP-1 activation. Our results indicated that while the down-regulation of novel PKC (nPKC) and conventional PKC (cPKC) by pretreatment of cells with 12-O-tetradecanoyl phorbol-13-actetate cannot block UVB-induced AP-1 activity, it can block 12-O-tetradecanoyl phorbol-13-acetate-induced AP-1 activity. Further, the dominant negative mutant PKCλ/l blocked UVB-induced AP-1 activity in all doses and time courses studied. In contrast, UVB- induced AP-1 activity from cells devoid of EGF receptor (B82) was not significantly different from that of the stable transfectants with a kinase- deficient EGF receptor (B82M721) or those with a wild-type EGF receptor (B82L) at all UVB irradiation doses and time courses studied. All of this evidence indicated that aPKC, but not EGF receptor, is involved in UVB- induced AP-1 activation.

Original languageEnglish (US)
Pages (from-to)31262-31268
Number of pages7
JournalJournal of Biological Chemistry
Volume271
Issue number49
DOIs
StatePublished - Dec 17 1996

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