Involvement of protein kinase C and Rho GTPase in the nuclear signalling pathway by transforming growth factor-β1 in rat-2 fibroblast cells

Sung E. Choi; Eui Yul Choi; Pyeung Hyeun Kim; Jae Hong Kim

doi:10.1016/S0898-6568(98)00033-3

Involvement of protein kinase C and Rho GTPase in the nuclear signalling pathway by transforming growth factor-β1 in rat-2 fibroblast cells

Sung E. Choi, Eui Yul Choi, Pyeung Hyeun Kim, Jae Hong Kim

Research output: Contribution to journal › Article › peer-review

22 Citations (Scopus)

Abstract

The transforming growth factor (TGF)-β signal-transduction cascade from the cell membrane to the nuclear target is poorly characterised. Here we report that treatment with TGF-β1 induces the levels of endogenous c-fos mRNA in Rat-2 fibroblast cells. In addition, by transient transfection analysis, TGF-β1 was shown to stimulate c-fos serum response element (SRE)-driven reporter gene activity in a dose- and time-dependent manner, suggesting that SRE is one of the nuclear targets of TGF-β1. To understand the signalling cascade by which TGF-β1 mediates the transactivation of c-fos SRE, cells were either pre-treated with various inhibitors or co-transfected with expression plasmids encoding inhibitory proteins for Rho GTPase together with the SRE-luciferase reporter gene. Our results showed that an inhibition of protein kinase C (PKC) or RhoA selectively repressed the stimulation of c-fos SRE by TGF-β1, implying the possible roles of PKC and RhoA GTPase in TGF-β1-induced signalling to c-fos SRE. Copyright (C) 1998 Elsevier Science Inc.

Original language	English
Pages (from-to)	71-76
Number of pages	6
Journal	Cellular Signalling
Volume	11
Issue number	1
DOIs	https://doi.org/10.1016/S0898-6568(98)00033-3
Publication status	Published - 1999 Jan
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by the Basic Science Research Institute Program, Ministry of Education, Korea, 1996, Project No. BSRI-96-4401 (to P. H. Kim) and by a grant from Hallym Academy of Sciences, Hallym University (to J. H. Kim).

Keywords

MAP kinase
PKC
Rho
SRE
Signal transduction
TGF-β
c-fos

ASJC Scopus subject areas

Cell Biology

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10.1016/S0898-6568(98)00033-3

Cite this

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title = "Involvement of protein kinase C and Rho GTPase in the nuclear signalling pathway by transforming growth factor-β1 in rat-2 fibroblast cells",

abstract = "The transforming growth factor (TGF)-β signal-transduction cascade from the cell membrane to the nuclear target is poorly characterised. Here we report that treatment with TGF-β1 induces the levels of endogenous c-fos mRNA in Rat-2 fibroblast cells. In addition, by transient transfection analysis, TGF-β1 was shown to stimulate c-fos serum response element (SRE)-driven reporter gene activity in a dose- and time-dependent manner, suggesting that SRE is one of the nuclear targets of TGF-β1. To understand the signalling cascade by which TGF-β1 mediates the transactivation of c-fos SRE, cells were either pre-treated with various inhibitors or co-transfected with expression plasmids encoding inhibitory proteins for Rho GTPase together with the SRE-luciferase reporter gene. Our results showed that an inhibition of protein kinase C (PKC) or RhoA selectively repressed the stimulation of c-fos SRE by TGF-β1, implying the possible roles of PKC and RhoA GTPase in TGF-β1-induced signalling to c-fos SRE. Copyright (C) 1998 Elsevier Science Inc.",

keywords = "MAP kinase, PKC, Rho, SRE, Signal transduction, TGF-β, c-fos",

author = "Choi, {Sung E.} and Choi, {Eui Yul} and Kim, {Pyeung Hyeun} and Kim, {Jae Hong}",

note = "Funding Information: This work was supported by the Basic Science Research Institute Program, Ministry of Education, Korea, 1996, Project No. BSRI-96-4401 (to P. H. Kim) and by a grant from Hallym Academy of Sciences, Hallym University (to J. H. Kim).",

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AU - Kim, Pyeung Hyeun

AU - Kim, Jae Hong

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N2 - The transforming growth factor (TGF)-β signal-transduction cascade from the cell membrane to the nuclear target is poorly characterised. Here we report that treatment with TGF-β1 induces the levels of endogenous c-fos mRNA in Rat-2 fibroblast cells. In addition, by transient transfection analysis, TGF-β1 was shown to stimulate c-fos serum response element (SRE)-driven reporter gene activity in a dose- and time-dependent manner, suggesting that SRE is one of the nuclear targets of TGF-β1. To understand the signalling cascade by which TGF-β1 mediates the transactivation of c-fos SRE, cells were either pre-treated with various inhibitors or co-transfected with expression plasmids encoding inhibitory proteins for Rho GTPase together with the SRE-luciferase reporter gene. Our results showed that an inhibition of protein kinase C (PKC) or RhoA selectively repressed the stimulation of c-fos SRE by TGF-β1, implying the possible roles of PKC and RhoA GTPase in TGF-β1-induced signalling to c-fos SRE. Copyright (C) 1998 Elsevier Science Inc.

AB - The transforming growth factor (TGF)-β signal-transduction cascade from the cell membrane to the nuclear target is poorly characterised. Here we report that treatment with TGF-β1 induces the levels of endogenous c-fos mRNA in Rat-2 fibroblast cells. In addition, by transient transfection analysis, TGF-β1 was shown to stimulate c-fos serum response element (SRE)-driven reporter gene activity in a dose- and time-dependent manner, suggesting that SRE is one of the nuclear targets of TGF-β1. To understand the signalling cascade by which TGF-β1 mediates the transactivation of c-fos SRE, cells were either pre-treated with various inhibitors or co-transfected with expression plasmids encoding inhibitory proteins for Rho GTPase together with the SRE-luciferase reporter gene. Our results showed that an inhibition of protein kinase C (PKC) or RhoA selectively repressed the stimulation of c-fos SRE by TGF-β1, implying the possible roles of PKC and RhoA GTPase in TGF-β1-induced signalling to c-fos SRE. Copyright (C) 1998 Elsevier Science Inc.

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Involvement of protein kinase C and Rho GTPase in the nuclear signalling pathway by transforming growth factor-β1 in rat-2 fibroblast cells

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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