Papillomavirus binding factor (PBF)-mediated inhibition of cell growth is regulated by 14-3-3beta

Nadine Sichtig1, Steffi Silling, Gertrud Steger

  • 1Institute of Virology, University of Cologne, Fürst-Pückler-Strasse 56, 50935 Cologne, Germany.

Insights

Papillomavirus (PV)-binding factor (PBF) interacts with 14-3-3beta, influencing cell growth. This interaction is regulated by PI3K/Akt signaling, revealing PBF

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Papillomavirus (PV)-binding factor (PBF), also known as Huntington's disease binding protein 2 (HDBP2), is a novel nuclear-shuttling transcription factor.
  • Its precise function and regulatory mechanisms remain largely uncharacterized.

Purpose of the Study:

  • To elucidate the function and regulation of PBF.
  • To identify PBF interaction partners and understand their role in cellular processes.

Main Methods:

  • Yeast two-hybrid screening to identify PBF interacting proteins.
  • Co-immunoprecipitation assays to confirm PBF-14-3-3beta interaction.
  • Kinase assays to investigate phosphorylation of PBF motifs.
  • Cellular localization studies and cell growth assays.

Main Results:

  • Identified 14-3-3beta as a PBF interaction partner, binding through specific motifs.
  • Demonstrated that PI3K/Akt signaling pathway kinases phosphorylate these motifs, facilitating PBF-14-3-3beta association.
  • Observed that PBF regulates cell growth, with overexpression inhibiting growth, an effect enhanced by a 14-3-3 binding-deficient mutant.

Conclusions:

  • Characterized PBF as a novel cellular factor involved in mediating the effects of PI3K/Akt signaling and 14-3-3 proteins on cell growth.
  • The PBF-14-3-3beta interaction plays a role in regulating PBF's subcellular localization and cellular function.

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