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Updated: Jun 17, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

c-Jun N-terminal kinase enhances MST1-mediated pro-apoptotic signaling through phosphorylation at serine 82

Wenzhi Bi1, Lei Xiao, Yunfeng Jia

  • 1National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

The Journal of Biological Chemistry
|December 24, 2009
PubMed

Insights

This study reveals that c-Jun N-terminal kinase (JNK) activates the MST1 kinase by phosphorylating it. This activation promotes cell death signaling, offering new insights into apoptosis regulation.

Area of Science:

  • Cellular biology
  • Molecular signaling
  • Apoptosis research

Background:

  • Protein kinases are crucial for cell survival and apoptosis balance.
  • Dysregulation of kinases contributes to diseases like cancer and neurodegeneration.
  • MST1 kinase is involved in apoptosis but its upstream regulation is unclear.

Purpose of the Study:

  • To identify upstream regulators of MST1 kinase.
  • To elucidate the mechanism of MST1 activation in apoptosis.
  • To investigate the role of JNK in MST1 signaling.

Main Methods:

  • Investigated the interaction between JNK and MST1.
  • Utilized site-directed mutagenesis (S82A) to assess MST1 phosphorylation.
  • Examined the effects of JNK inhibition on MST1 activity and apoptosis.

Main Results:

  • JNK phosphorylates MST1 at serine 82, enhancing its activation.
  • Activated MST1 phosphorylates FOXO3, promoting cell death.
  • Inhibition of JNK reduces MST1 activity and MST1-induced apoptosis.
  • Mutation of serine 82 to alanine impairs MST1 activation and FOXO transcription activity.

Conclusions:

  • JNK acts as a novel upstream activator of MST1 kinase through phosphorylation.
  • This JNK-MST1 interaction represents a feedback loop in cell death signaling.
  • Findings enhance understanding of molecular mechanisms underlying apoptosis.

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