title: Synergistic stimulation of avian I kappa B alpha transcription by rel and fos/jun factors.
abstract: Rel/NF-kappa B transcription factors and I Kappa B alpha function in an autoregulatory network. Avian I kappa B alpha transcription is increased in response to both c-Rel and v-Rel. This study shows that I kappa B alpha transcription is synergistically stimulated by Rel and AP-1 factors (c-Fos and c-Jun). However, the response to v-Rel and the AP-1 factors was not as vigorous as that of c-Rel and AP-1. A 386 bp region of the I kappa B alpha promoter (containing two NF-kappa B and one AP-1 binding sites) was shown to be both necessary and sufficient for response to both Rel factors alone or Rel factors in conjunction with the AP-1 proteins. In addition, an imperfect NF-kappa B binding site was found to overlap the AP-1 binding site. Mutation of either of the NF-kappa B binding sites or the AP-1 binding site dramatically decreased the response of the I kappa B alpha promoter to Rel proteins alone or Rel and AP-1 factors. Overexpression of c-Rel or v-Rel resulted in the formation of DNA binding complexes associated with the imperfect NF-kappa B binding site which overlaps the AP-1 site. v-Rel associated with the imperfect NF-kappa B site stronger than c-Rel, and overexpression of v-Rel also resulted in the formation of a v-Rel containing complex bound to a consensus AP-1 site. These studies address the difference in c-Rel and v-Rel's ability to synergistically stimulate I kappa B alpha expression in conjunction with the AP-1 factors.
authors.affiliation: Department of Microbiology and the Cell Research Institute, University of Texas at Austin, Austin, TX 78712-1095, USA.
authors.forename: J
authors.initials: J
authors.lastname: Kralova
authors.forename: J D
authors.initials: JD
authors.lastname: Schatzle
authors.forename: A S
authors.initials: AS
authors.lastname: Liss
authors.forename: W
authors.initials: W
authors.lastname: Bargmann
authors.forename: H R
authors.initials: HR
authors.lastname: Bose
mesh_terms: D000818:Animals; D001483:Base Sequence; D001665:Binding Sites; D002642:Chick Embryo; D004252:DNA Mutational Analysis; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D017930:Genes, Reporter; D016762:Genes, fos; D016758:Genes, jun; D020672:I-kappa B Proteins; D008156:Luciferases / Q000235:genetics; D008969:Molecular Sequence Data; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D020572:Oncogene Proteins v-rel; D011401:Promoter Regions, Genetic; D011518:Proto-Oncogene Proteins / Q000235:genetics; D020569:Proto-Oncogene Proteins c-rel; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D015682:Retroviridae Proteins, Oncogenic / Q000235:genetics*; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic
chemical_list: D004268:DNA-Binding Proteins; D020672:I-kappa B Proteins; D016328:NF-kappa B; D020572:Oncogene Proteins v-rel; D011518:Proto-Oncogene Proteins; D020569:Proto-Oncogene Proteins c-rel; D011994:Recombinant Proteins; D015682:Retroviridae Proteins, Oncogenic; D018808:Transcription Factor AP-1; D000072000:NF-KappaB Inhibitor alpha; D008156:Luciferases