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
. 1993 Sep;12(9):3551-8.
doi: 10.1002/j.1460-2075.1993.tb06029.x.

A cooperative interaction between NF-kappa B and Sp1 is required for HIV-1 enhancer activation

Affiliations

A cooperative interaction between NF-kappa B and Sp1 is required for HIV-1 enhancer activation

N D Perkins et al. EMBO J. 1993 Sep.

Abstract

The human immunodeficiency virus (HIV-1) long terminal repeat (LTR) contains two binding sites for NF-kappa B in close proximity to three binding sites for the constitutive transcription factor, Sp1. Previously, stimulation of the HIV enhancer in response to mitogens has been attributed to the binding of NF-kappa B to the viral enhancer. In this report, we show that the binding of NF-kappa B is not by itself sufficient to induce HIV gene expression. Instead, a protein-protein interaction must occur between NF-kappa B and Sp1 bound to an adjacent site. Cooperativity both in DNA binding and in transcriptional activation of NF-kappa B and Sp1 was confirmed by electrophoretic mobility shift gel analysis, DNase footprinting, chemical cross-linking and transfection studies in vivo. With a heterologous promoter, we find that the interaction of NF-kappa B with Sp1 is dependent on orientation and position, and is not observed with other elements, including GATA, CCAAT or octamer. An increase in the spacing between the kappa B and Sp1 elements virtually abolishes this functional interaction, which is not restored when these sites are brought back into the same helical position. Several other promoters regulated by NF-kappa B also contain kappa B in proximity to Sp1 binding sites. These findings suggest that an interaction between NF-kappa B and Sp1 is required for inducible HIV-1 gene expression and may serve as a regulatory mechanism to activate specific viral and cellular genes.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Nature. 1990 Nov 1;348(6296):76-80 - PubMed
    1. J Virol. 1991 Aug;65(8):4350-8 - PubMed
    1. Nature. 1986 Feb 13-19;319(6054):555-9 - PubMed
    1. Science. 1986 May 9;232(4751):755-9 - PubMed
    1. Cell. 1986 Dec 26;47(6):921-8 - PubMed

MeSH terms

  NODES
chat 1
INTERN 2
twitter 2