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Updated: Aug 21, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53 suppresses c-Myb-induced trans-activation and transformation by recruiting the corepressor mSin3A

Jun Tanikawa1, Teruaki Nomura, Elizabeth M Macmillan

  • 1Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.

The Journal of Biological Chemistry
|October 29, 2004
PubMed

Insights

The tumor suppressor p53 directly binds to the c-Myb protein, inhibiting its function in cell proliferation. This interaction recruits a corepressor, leading to the down-regulation of specific genes targeted by c-Myb.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The p53 protein is a known transcriptional repressor, but the mechanisms of its gene recruitment are unclear.
  • The c-Myb proto-oncogene product (c-Myb) promotes the proliferation of immature hematopoietic cells, while p53 inhibits cell cycle progression.

Purpose of the Study:

  • To investigate the mechanism by which p53 inhibits c-Myb-induced transcription and transformation.
  • To elucidate the molecular interaction between p53 and c-Myb.

Main Methods:

  • Direct binding assays to confirm interaction between p53 and c-Myb.
  • Analysis of c-Myb DNA binding ability in the presence of p53.
  • Ternary complex formation studies involving p53, c-Myb, and mSin3A.
  • Assessment of M1 cell differentiation and proliferation.

Main Results:

  • p53 directly binds to c-Myb, inhibiting its transcriptional activity and transforming potential.
  • p53 suppresses the ability of c-Myb to maintain the undifferentiated state of M1 cells.
  • p53 does not impede c-Myb's DNA binding but forms a ternary complex with c-Myb and the corepressor mSin3A.

Conclusions:

  • p53 antagonizes c-Myb function through direct protein-protein interaction.
  • p53 recruits the corepressor mSin3A to c-Myb, leading to the down-regulation of specific Myb target genes.
  • This mechanism provides insight into how p53 regulates hematopoietic cell proliferation and differentiation.

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