Mapping of polyomavirus middle T domain that is responsible for AP-1 activation

Maria Leonor S. Oliveira, Thomas M. Roberts, Brian J. Druker, Mari C.S. Armelin

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Cell transformation by Polyomavirus middle T (MT) oncoprotein involves binding and activation of several cytoplasmic proteins that participate in growth factors-induced mitogenic signal transduction to the nucleus. We have previously reported that the AP-1 transcriptional complex is a target for MT during cell transformation. To analyse the interactions between MT and cellular proteins that are required for constitutive AP-1 activation, we compared wild type and transformation-defective MT mutant cell lines. High AP-1 activity, assessed by gel mobility shift assays, displayed by MT-overexpressing cells, is dependent on MT binding to phosphatidylinositol-3 kinase (P13K). Treatment with wortmannin (a specific P13K inhibitor) leads to decreased AP-1 activity. Super-shift and Western blot analysis with specific antisera, indicate that JunB and cJun, but not cFos or FosB are present in the AP-1 complex. The results confirm the AP-1 complex as a downstream MT target and indicate that AP-1 activation may not be sufficient for cell transformation, since two transformation-defective MT mutants (250phe and MT322) display high AP-1 activity.

Original languageEnglish (US)
Pages (from-to)2975-2982
Number of pages8
JournalOncogene
Volume16
Issue number23
DOIs
StatePublished - Jun 11 1998

Keywords

  • AP-1 activation phosphatidylinositol-3 kinase
  • Cell transformation
  • Middle T antigen
  • Polyomavirus

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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