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Transforming growth factor beta stimulates the human immunodeficiency virus 1 enhancer and requires NF-kappaB activity.

Publication ,  Journal Article
Li, JM; Shen, X; Hu, PP; Wang, XF
Published in: Mol Cell Biol
January 1998

Transforming growth factor beta (TGF-beta) is the prototype of a large superfamily of signaling molecules involved in the regulation of cell growth and differentiation. In certain patients infected with human immunodeficiency virus type 1 (HIV-1), increased levels of TGF-beta promoted the production of virus and also impaired the host immune system. In an effort to understand the signaling events linking TGF-beta action and HIV production, we show here that TGF-beta can stimulate transcription from the HIV-1 long terminal repeat (LTR) promoter through NF-kappaB binding sites in both HaCaT and 300.19 pre-B cells. When introduced into a minimal promoter, NF-kappaB binding sites supported nearly 30-fold activation from the luciferase reporter upon TGF-beta treatment. Electrophoretic mobility shift assay indicated that a major factor binding to the NF-kappaB site is the p50-p65 heterodimeric NF-kappaB in HaCaT cells. Coexpression of Gal4-p65 chimeric proteins supported TGF-beta ligand-dependent gene expression from a luciferase reporter gene driven by Gal4 DNA binding sites. NF-kappaB activity present in HaCaT cells was not affected by TGF-beta treatment as judged by the unchanged DNA binding activity and concentrations of p50 and p65 proteins. Consistently, steady-state levels of IkappaB alpha and IkappaB beta proteins were not changed by TGF-beta treatment. Our results demonstrate that TGF-beta is able to stimulate transcription from the HIV-1 LTR promoter by activating NF-kappaB through a mechanism distinct from the classic NF-kappaB activation mechanism involving the degradation of IkappaB proteins.

Duke Scholars

Published In

Mol Cell Biol

DOI

ISSN

0270-7306

Publication Date

January 1998

Volume

18

Issue

1

Start / End Page

110 / 121

Location

United States

Related Subject Headings

  • Transforming Growth Factor beta
  • Transcriptional Activation
  • NF-kappa B
  • Humans
  • HIV-1
  • HIV Long Terminal Repeat
  • HIV Infections
  • Enhancer Elements, Genetic
  • Developmental Biology
  • Cell Line
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Li, J. M., Shen, X., Hu, P. P., & Wang, X. F. (1998). Transforming growth factor beta stimulates the human immunodeficiency virus 1 enhancer and requires NF-kappaB activity. Mol Cell Biol, 18(1), 110–121. https://doi.org/10.1128/MCB.18.1.110
Li, J. M., X. Shen, P. P. Hu, and X. F. Wang. “Transforming growth factor beta stimulates the human immunodeficiency virus 1 enhancer and requires NF-kappaB activity.Mol Cell Biol 18, no. 1 (January 1998): 110–21. https://doi.org/10.1128/MCB.18.1.110.
Li, J. M., et al. “Transforming growth factor beta stimulates the human immunodeficiency virus 1 enhancer and requires NF-kappaB activity.Mol Cell Biol, vol. 18, no. 1, Jan. 1998, pp. 110–21. Pubmed, doi:10.1128/MCB.18.1.110.

Published In

Mol Cell Biol

DOI

ISSN

0270-7306

Publication Date

January 1998

Volume

18

Issue

1

Start / End Page

110 / 121

Location

United States

Related Subject Headings

  • Transforming Growth Factor beta
  • Transcriptional Activation
  • NF-kappa B
  • Humans
  • HIV-1
  • HIV Long Terminal Repeat
  • HIV Infections
  • Enhancer Elements, Genetic
  • Developmental Biology
  • Cell Line