Distinct NF-kappa B/Rel transcription factors are responsible for tissue-specific and inducible gene activation

Nature. 1993 Oct 21;365(6448):767-70. doi: 10.1038/365767a0.


The NF-kappa B/Rel family is a growing class of transcriptional regulators whose members share the conserved Rel-homology domain, involved in specific DNA binding and dimerization. They interact with the regulatory elements of many different genes and are involved in the regulation of lymphoid-specific and inducible transcription. We tested whether these factors could alone activate a gene in transgenic mice. We report here that a minimal promoter containing three copies of a binding site for these proteins allows tissue-specific and inducible transgene activation. In lymphoid tissues constitutive transgene expression correlates with the presence of a constitutively active p50/RelB heterodimer. Other organs that only contain the p50 homodimer do not express the transgene. In contrast to this constitutive activity mediated by p50/RelB, the p50/p65 heterodimer (which is NF-kappa B) could confer inducible transgene activation in embryo fibroblasts. Thus two different members of the NF-kappa B/Rel family of transcriptional activators are involved in tissue-specific and inducible gene activation in transgenic mice.

MeSH terms

  • Animals
  • B-Lymphocytes / metabolism
  • Base Sequence
  • Binding Sites
  • Cell Line
  • Cells, Cultured
  • DNA Primers
  • Embryo, Mammalian / cytology
  • Gene Expression Regulation*
  • Genes, Reporter
  • Globins / genetics
  • Lymphoid Tissue / cytology
  • Lymphoid Tissue / metabolism
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • NF-kappa B / physiology*
  • NF-kappa B p50 Subunit
  • RNA / metabolism
  • Spleen / metabolism
  • T-Lymphocytes / metabolism
  • Transcription Factor RelA
  • Transcriptional Activation
  • Tumor Necrosis Factor-alpha / pharmacology


  • DNA Primers
  • NF-kappa B
  • NF-kappa B p50 Subunit
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • RNA
  • Globins