Induction of interleukin-2 receptor-alpha gene expression is regulated by post-translational activation of kappa B specific DNA binding proteins

J Biol Chem. 1989 May 25;264(15):8475-8.


T cell mitogens induce the expression of specific trans-acting DNA binding proteins that in turn regulate the expression of the interleukin-2 receptor-alpha (IL-2R alpha) gene. To investigate whether de novo protein synthesis is required for the activation of these transacting factors and the induced expression of this receptor gene, Jurkat T cells were incubated with various inhibitors of protein synthesis prior to stimulation with phytohemagglutinin and phorbol 12-myristate 13-acetate (PMA). Despite the presence of cycloheximide or anisomycin at concentrations sufficient to block greater than 97% of cellular protein synthesis, phytohemagglutinin and phorbol 12-myristate 13-acetate effectively induced the expression of the IL-2R alpha gene as measured at the mRNA level. Similarly, gel retardation, DNA footprinting, and DNA-protein cross-linking studies revealed that these mitogens induced the activation of two predominant DNA binding proteins (50-55 and 80-90 kDa) in the presence or absence of cycloheximide and anisomycin. Both of these proteins specifically interacted with a kappa B-like binding site present in the IL-2R alpha promoter (-267 to -256) that is requisite for mitogen-induced expression of this receptor gene. These findings support a post-translational mechanism of induction of pre-existing, but inactive, DNA binding proteins which in turn bind to and activate the IL-2R alpha gene.

MeSH terms

  • Blotting, Northern
  • Cell Line
  • DNA-Binding Proteins / genetics*
  • Gene Expression Regulation* / drug effects
  • Genes*
  • Humans
  • Interleukin-2 / metabolism*
  • Lymphocyte Activation
  • Nuclear Proteins / metabolism
  • Protein Processing, Post-Translational*
  • Protein Synthesis Inhibitors / pharmacology
  • Receptors, Interleukin-2 / biosynthesis
  • Receptors, Interleukin-2 / genetics*
  • T-Lymphocytes
  • Transcription, Genetic


  • DNA-Binding Proteins
  • Interleukin-2
  • Nuclear Proteins
  • Protein Synthesis Inhibitors
  • Receptors, Interleukin-2