TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y

FEBS Lett. 2001 Oct 12;506(3):267-71. doi: 10.1016/s0014-5793(01)02928-3.

Abstract

The JunB gene is activated by many stimuli including transforming growth factor beta (TGFbeta) family members and interleukin-6 (IL-6). Here the effect of TGFbeta activated kinase 1 (TAK1), a mitogen activated protein kinase kinase kinase (MAPKKK) implicated in TGFbeta, bone morphogenetic protein (BMP) and interleukin-1 (IL-1) signaling, on JunB promoter activity was investigated. Promoter analysis led to the identification of a CCAAT motif in the JunB gene, essential for activation by TAK1. Transfer of this CCAAT element to a heterologous minimal promoter conferred TAK1-responsiveness. The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), activated the JunB promoter and a dominant negative NF-YA construct inhibited TAK1 activation of JunB. Our results demonstrate that JunB gene activation by TAK1 is mediated by the CCAAT-binding factor NF-Y.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • CCAAT-Binding Factor / metabolism*
  • Cell Line
  • DNA
  • DNA Primers
  • Gene Expression Regulation / genetics
  • Genes, Reporter
  • Humans
  • Interleukin-1 / physiology
  • Luciferases / genetics
  • MAP Kinase Kinase Kinases / metabolism*
  • Mice
  • Promoter Regions, Genetic*
  • Proto-Oncogene Proteins c-jun / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcriptional Activation
  • Transforming Growth Factor beta / physiology

Substances

  • CCAAT-Binding Factor
  • DNA Primers
  • Interleukin-1
  • Proto-Oncogene Proteins c-jun
  • Transforming Growth Factor beta
  • DNA
  • Luciferases
  • MAP Kinase Kinase Kinases
  • MAP kinase kinase kinase 7