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JNK1 inhibits transcriptional and pro-apoptotic activity of TAp63γ

Ji Chen1, Hua Shi2, Jin Qi3

  • 1Center of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Chengdu 610065, China; Department of Medical Oncology, The Seventh People's Hospital of Chengdu, Chengdu 610041, China.

FEBS Letters
|November 1, 2015
PubMed

Insights

JNK1 kinase inhibits the tumor suppressor TAp63γ by interacting with its transactivation domain. This interaction impairs TAp63γ

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • TAp63γ is a homologue of the tumor suppressor p53.
  • TAp63γ acts as a transcriptional factor involved in cell cycle regulation and apoptosis.

Purpose of the Study:

  • To investigate the interaction between JNK1 and TAp63γ.
  • To elucidate the regulatory mechanism of TAp63γ activity by JNK1.

Main Methods:

  • Co-immunoprecipitation assays to confirm physical interaction.
  • Reporter assays to measure transcriptional activity.
  • Site-directed mutagenesis to identify critical residues.
  • Western blotting to assess protein levels.

Main Results:

  • JNK1 physically interacts with the N-terminal transactivation domain (TAD) of TAp63γ.
  • JNK1 overexpression inhibits TAp63γ-mediated transcription.
  • Knockdown or inhibition of JNK1 enhances TAp63γ transactivity.
  • Serine 12 (Ser12) in the TAD is crucial for JNK1-mediated inhibition.
  • JNK1-mediated inhibition impairs the pro-apoptotic function of TAp63γ.

Conclusions:

  • JNK1 negatively regulates TAp63γ transcriptional activity and pro-apoptotic function.
  • The interaction between JNK1 and TAp63γ at Ser12 is critical for this regulation.
  • This study reveals a novel regulatory pathway for TAp63γ.
Keywords:
ApoptosisTAp63γTransactivityc-Jun N-terminal kinase 1

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