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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
1996-9-4
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pubmed:abstractText |
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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappaB inhibitor alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins v-rel,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-rel,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Retroviridae Proteins, Oncogenic,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2595-604
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8700518-Animals,
pubmed-meshheading:8700518-Base Sequence,
pubmed-meshheading:8700518-Binding Sites,
pubmed-meshheading:8700518-Chick Embryo,
pubmed-meshheading:8700518-DNA Mutational Analysis,
pubmed-meshheading:8700518-DNA-Binding Proteins,
pubmed-meshheading:8700518-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:8700518-Genes, Reporter,
pubmed-meshheading:8700518-Genes, fos,
pubmed-meshheading:8700518-Genes, jun,
pubmed-meshheading:8700518-I-kappa B Proteins,
pubmed-meshheading:8700518-Luciferases,
pubmed-meshheading:8700518-Molecular Sequence Data,
pubmed-meshheading:8700518-NF-kappa B,
pubmed-meshheading:8700518-Oncogene Proteins v-rel,
pubmed-meshheading:8700518-Promoter Regions, Genetic,
pubmed-meshheading:8700518-Proto-Oncogene Proteins,
pubmed-meshheading:8700518-Proto-Oncogene Proteins c-rel,
pubmed-meshheading:8700518-Recombinant Proteins,
pubmed-meshheading:8700518-Retroviridae Proteins, Oncogenic,
pubmed-meshheading:8700518-Transcription, Genetic,
pubmed-meshheading:8700518-Transcription Factor AP-1
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pubmed:year |
1996
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pubmed:articleTitle |
Synergistic stimulation of avian I kappa B alpha transcription by rel and fos/jun factors.
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pubmed:affiliation |
Department of Microbiology and the Cell Research Institute, University of Texas at Austin, Austin, TX 78712-1095, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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