NF-IL6-mediated transcriptional activation of the long terminal repeat of the human immunodeficiency virus type 1 Academic Article uri icon

Overview

MeSH Major

  • DNA-Binding Proteins
  • Gene Expression Regulation, Viral
  • HIV Long Terminal Repeat
  • HIV-1
  • Nuclear Proteins
  • Transcriptional Activation

abstract

  • An upstream control region in the long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) includes a potential negative regulatory element (NRE1). Cotransfecting multimers of a sequence spanning this element with an LTR-CAT construct produced an increase in chloramphenicol acetyltransferase (CAT) activity in Jurkat and HepG2 cells, providing further evidence and support for the existence of an NRE. In screening experiments aimed at identifying those factors that regulate HIV-1 transcription through interactions with the NRE1 region, we isolated a cDNA for NF-IL6. Previous studies have shown that NF-IL6 is a key nuclear factor that activates gene expression in response to interleukin 6. By methylation interference analysis, we have localized the NF-IL6 binding site within the NRE1 region and found that it overlaps an E box that has previously been implicated as the binding element for a negative regulator of HIV-1 expression. Through a database search, we identified an additional consensus binding sequence for NF-IL6 in the LTR of many HIV-1 variants and found that over this sequence, purified NF-IL6 can produce an extended footprint that overlaps one of the binding sites for NF-kappa B. A product of the nf-il6 gene activated transcription from several LTR-CAT constructs in transient transfection assays. Thus, NF-IL6 could play a central role in the control of HIV-1 gene expression and this protein might be a key mediator in signaling pathways where HIV-1 is activated by interleukin 6.

publication date

  • August 1993

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC47124

PubMed ID

  • 8346247

Additional Document Info

start page

  • 7298

end page

  • 302

volume

  • 90

number

  • 15