Characterization and functional analysis of the p42Ets-1 variant of the mouse Ets-1 transcription factor

Frédéric Lionneton, Etienne Lelièvre, David Baillat, Dominique Stehelin, Fabrice Soncin

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

We have identified the mouse exon VII splice variant of the Ets-1 transcription factor. The variant is expressed in all cell lines which express ets-1, at lower levels, it is also expressed in the mouse embryo in vivo. The corresponding protein, p42Ets-1, is a transcription factor as it is able to bind to specific DNA sequences and to transactivate a bona fide ETS reporter vector. A comparison of optimal DNA-binding sites shows that p42Ets-1 binds to more various DNA sequences than p51Ets-1; p42Ets-1 recognizes the same optimal consensus sequence as p51Ets-1, but also many variations of it, mainly at base -1, which is located just prior to the GGAA/T core sequence. The binding differences were quantified by surface plasmon resonance analyses and the protein region responsible for the differences in DNA sequence recognition located in the Val280-Glu302 fragment, which is encoded by exon VII. The specific DNA-binding properties of each isoform translates into clear differences in activity, p42Ets-1 transactivates the natural VE-cadherin gene promoter through both ETS-binding site (EBS)2 and EBS4 whereas p51Ets-1 is mainly active on EBS4. Altogether, our data suggest that p42Ets-1 acts as a distinct transcription factor from p51Ets-1.

Original languageEnglish (US)
Pages (from-to)9156-9164
Number of pages9
JournalOncogene
Volume22
Issue number57
DOIs
StatePublished - Dec 11 2003

Keywords

  • Endothelium
  • Ets-1
  • Gene promoter
  • VE-cadherin

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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    Lionneton, F., Lelièvre, E., Baillat, D., Stehelin, D., & Soncin, F. (2003). Characterization and functional analysis of the p42Ets-1 variant of the mouse Ets-1 transcription factor. Oncogene, 22(57), 9156-9164. https://doi.org/10.1038/sj.onc.1207241