Overexpression of RelB in transgenic mice does not affect I kappa B alpha levels: differential regulation of RelA and RelB by the inhibitor protein

Oncogene. 1996 Jan 18;12(2):445-9.

Abstract

In mouse lymphoid tissues, RelB heterodimers represent the constitutive kappa B-binding activity, whereas RelA and c-Rel complexes most likely are involved in inducible kappa B-binding and gene activation. Our laboratory has previously shown that the potential excess of NF-kappa B activity in transgenic mice overexpressing RelA is counteracted by a dramatic increase in I kappa B alpha, mainly due to its increased stability through association with RelA. As an attempt to elucidate the in vivo mechanisms that lead to the constitutive DNA-binding activity of RelB heterodimers, we have generated mouse lines overexpressing a relB transgene in a position-independent and copy number-dependent manner. Expression of RelB in these transgenic animals is very high in immature thymocytes and restricted to T cell areas in secondary lymphoid tissues. In contrast to the results obtained with RelA-transgenic thymocytes, we demonstrate here that overexpression of RelB results in a dramatic increase in overall kappa B-binding activity. Interestingly, I kappa B alpha protein levels are not altered in the RelB-transgenic animals, indicating that within the same cell type RelA and RelB complexes are differentially regulated by I kappa B alpha.

MeSH terms

  • Animals
  • DNA-Binding Proteins / physiology*
  • I-kappa B Proteins*
  • Mice
  • Mice, Transgenic
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / physiology*
  • Proto-Oncogene Proteins*
  • Transcription Factor RelA
  • Transcription Factor RelB
  • Transcription Factors / genetics
  • Transcription Factors / physiology*

Substances

  • DNA-Binding Proteins
  • I-kappa B Proteins
  • NF-kappa B
  • Nfkbia protein, mouse
  • Proto-Oncogene Proteins
  • Relb protein, mouse
  • Transcription Factor RelA
  • Transcription Factors
  • NF-KappaB Inhibitor alpha
  • Transcription Factor RelB