Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1994 May 15;13(10):2331-40.
doi: 10.1002/j.1460-2075.1994.tb06517.x.

Ras-dependent signal transduction is indispensable but not sufficient for the activation of AP1/Jun by PKC delta

S Hirai  1 , Y Izumi, K Higa, K Kaibuchi, K Mizuno, S Osada, K Suzuki, S Ohno
Affiliations

Ras-dependent signal transduction is indispensable but not sufficient for the activation of AP1/Jun by PKC delta

S Hirai et al. EMBO J. .

Abstract

Modulation of gene expression by 12-O-tetradecanoylphorbol-13-acetate (TPA) is thought to be mediated by protein kinase C (PKC), a major cellular receptor for TPA. We confirm this by showing that the overexpression of PKC delta enhances the TPA induction of the TRE-tk-CAT reporter gene in NIH3T3 cells. To investigate the mutual relationship between PKC delta- and Ras-dependent signal transduction pathways to a TRE binding transcription factor, AP1/Jun, we constructed constitutively active and dominant negative mutants of PKC delta. Activated Ras induced reporter gene expression in collaboration with overexpressed c-Jun or JunD, and this induction was insensitive to the dominant negative PKC delta. On the other hand, reporter gene expression induced by the constitutively active PKC delta was severely inhibited by dominant negative Ras, as well as by the dominant negative PKC delta. Thus, Ras activation must be indispensable for PKC delta to activate AP1/Jun. In the absence of overexpressed c-Jun or JunD, activated Ras was, however, clearly less effective than constitutively active PKC delta which showed full activation of reporter gene expression by itself. This suggests the presence of an additional, Ras-independent, signaling pathway downstream of PKC delta to activate AP1/Jun. In spite of the remarkable ability of constitutively active PKC delta to activate TRE-tk-CAT expression, this mutant suppressed cell growth.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Science. 1987 Dec 18;238(4834):1726-8 - PubMed
    1. Proc Natl Acad Sci U S A. 1982 Nov;79(22):6777-81 - PubMed
    1. Cell. 1988 Apr 22;53(2):211-7 - PubMed
    1. J Biol Chem. 1988 May 15;263(14):6927-32 - PubMed
    1. Cell. 1988 Jun 3;53(5):731-41 - PubMed

Publication types

MeSH terms