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Structure and apoptotic function of p73

Mi-Kyung Yoon1, Ji-Hyang Ha1, Min-Sung Lee2

  • 1Structural Biology & Nanopore Research Laboratory, Functional Genomics Research Center, KRIBB, Daejeon 305-806, Korea.

BMB Reports
|December 3, 2014
PubMed

Insights

The p73 protein, a homolog of p53, induces apoptosis and cell cycle arrest, offering a therapeutic strategy for cancers with mutated p53. This review explores p73 structure and its apoptosis mechanisms.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Neuroscience

Background:

  • p73 is a homolog of the p53 tumor suppressor.
  • p73 shares functions with p53, including apoptosis induction and cell cycle arrest.
  • p73 has distinct roles in neuronal development and differentiation.

Purpose of the Study:

  • To review the structural characteristics of p73.
  • To compare the structures of p73 and p53.
  • To elucidate the molecular mechanisms underlying p73-induced apoptosis.

Main Methods:

  • Structural analysis of p73.
  • Comparative structural analysis of p73 and p53.
  • Review of literature on p73-mediated apoptosis.

Main Results:

  • p73 exhibits structural similarities and differences with p53.
  • p73-induced apoptosis can compensate for p53 loss in cancer cells.
  • Both transcription-dependent and -independent pathways mediate p73 apoptosis.

Conclusions:

  • Understanding p73 structure is crucial for cancer therapy.
  • p73 represents a potential therapeutic target for cancers with p53 mutations.
  • Further research into p73's molecular mechanisms is warranted.

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