Dominant-negative Smad-3 interferes with transcriptional activation by multiple agonists

I. Mucsi, Howard J. Goldberg

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Smad proteins have recently been identified as mediators of transcriptional activation by members of the transforming growth factor-β superfamily. To determine if Smads might also be involved in inducing gene transcription in response to other agonists, expression vectors for dominant-negative Smad proteins were constructed. These plasmids were transiently cotransfected with luciferase reporter genes and the effects of various agonists on reporter gene activity evaluated in NIH 3T3 cells. Dominant-negative Smad3, but not other dominant-negative Smads, reduced stimulation of the plasminogen activator inhibitor-1 (PAI-1) and other gene promoters by phorbol ester, cAMP, and platelet-derived growth factor. Activation of the PAI-1 promoter by TGF-β or prostaglandin F2α, and transactivation by c-Jun or JunB were not inhibited by dominant-negative Smads, supporting the specificity of this mutant. These results suggest that Smad3, like CREB-binding protein (CBP), may participate in transcriptional activation by multiple agonists.

Original languageEnglish
Pages (from-to)517-521
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume232
Issue number2
DOIs
Publication statusPublished - Mar 17 1997

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Smad Proteins
Transcriptional Activation
Genes
Chemical activation
Plasminogen Activator Inhibitor 1
Reporter Genes
CREB-Binding Protein
NIH 3T3 Cells
Dinoprost
Platelet-Derived Growth Factor
Transforming Growth Factors
Phorbol Esters
Luciferases
Plasmids
Transcription

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Dominant-negative Smad-3 interferes with transcriptional activation by multiple agonists. / Mucsi, I.; Goldberg, Howard J.

In: Biochemical and Biophysical Research Communications, Vol. 232, No. 2, 17.03.1997, p. 517-521.

Research output: Contribution to journalArticle

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