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CACUL1/CAC1 attenuates p53 activity through PML post-translational modification

Tomomi Fukuda1, Yu Kigoshi-Tansho1, Takao Naganuma2

  • 1Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.

Biochemical and Biophysical Research Communications
|November 28, 2016
PubMed

Insights

CACUL1 protein inhibits Promyelocytic leukaemia (PML) SUMOylation, impacting PML nuclear body size and negatively regulating p53 activity. This discovery reveals CACUL1 as a key factor in controlling cellular processes.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Promyelocytic leukaemia (PML) protein forms nuclear bodies (NBs) crucial for gene expression and chromatin integrity.
  • PML SUMOylation regulates diverse cellular functions, but its control mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of Cullin-related protein CACUL1 in regulating PML posttranslational modification and its impact on cellular functions.
  • To elucidate the interaction between CACUL1, PML, and Ubc9 in controlling PML SUMOylation and p53 activity.

Main Methods:

  • Co-immunoprecipitation assays to study protein-protein interactions.
  • Western blotting to analyze protein modification levels.
  • Analysis of PML nuclear body size and p53 transcriptional activity.

Main Results:

  • CACUL1 directly interacts with PML and inhibits its SUMOylation, affecting PML-NB size.
  • Ubc9 binds to CACUL1, antagonizing the CACUL1-PML interaction.
  • CACUL1 suppresses p53 transcriptional activity.

Conclusions:

  • CACUL1 acts as a novel negative regulator of p53 activity by controlling PML SUMOylation.
  • Understanding CACUL1's role in PML regulation offers insights into cancer biology and potential therapeutic targets.
Keywords:
CACUL1PMLSUMOUbiquitinp53

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