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p53 target DDA3 binds ASPP2 and inhibits its stimulation on p53-mediated BAX activation

Wei-Tzu Sun1, Pei-Chen Hsieh, Ming-Lun Chiang

  • 1Institute of Biochemistry and Molecular Biology, National Yang-Ming University, No. 155, Sec., 2 Linong Street, Taipei 112, Taiwan.

Biochemical and Biophysical Research Communications
|September 17, 2008
PubMed

Insights

The tumor suppressor p53 maintains genome integrity. Researchers found that DDA3, an oncoprotein, interacts with ASPP2, a p53 binding protein, potentially inhibiting p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The p53 tumor suppressor is crucial for maintaining genomic integrity.
  • DDA3 is an oncoprotein regulated by p53.
  • Understanding DDA3's function requires identifying its interacting partners.

Purpose of the Study:

  • To identify proteins interacting with DDA3.
  • To investigate the functional consequences of the DDA3-ASPP2 interaction on p53 signaling.

Main Methods:

  • Yeast two-hybrid screening to identify DDA3 interacting proteins.
  • In vitro GST pull-down assays to confirm protein binding.
  • In vivo immunofluorescence to assess protein colocalization.
  • Reporter assays to evaluate effects on p53-mediated gene activation.

Main Results:

  • ASPP2 was identified as a DDA3 binding partner.
  • DDA3 and ASPP2 binding was confirmed using biochemical and cellular assays.
  • The interaction domains within DDA3 and ASPP2 were mapped.
  • DDA3 inhibited ASPP2's ability to stimulate p53-mediated BAX promoter activity without disrupting ASPP2-p53 binding.

Conclusions:

  • ASPP2 is a genuine interacting protein of DDA3.
  • The DDA3-ASPP2 interaction negatively regulates ASPP2's role in promoting p53-dependent apoptosis.
  • This interaction may represent a novel mechanism for modulating tumor suppressor pathways.

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