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Activation of the JNK signaling pathway: breaking the brake on apoptosis

Anning Lin1

  • 1Ben May Institute for Cancer Research, The University of Chicago, 5841 S. Maryland Avenue, MC 6027, Chicago, Il 60637, USA. alin@huggins.bsd.uchicago.edu

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|January 1, 2003
PubMed

Insights

The JNK signaling pathway regulates apoptosis, but does not initiate it. Its role depends on cell type and stimulus, often interacting with pathways like NF-kappaB.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The c-Jun N-terminal kinase (JNK) signaling pathway regulates critical cellular processes.
  • JNK's role in apoptosis is debated, with evidence suggesting pro-apoptotic, anti-apoptotic, or no involvement.
  • JNK pathway activity is cell-type and stimulus-dependent, with components sometimes having opposing effects.

Purpose of the Study:

  • To propose a model explaining how JNK pathway activation influences apoptosis.
  • To clarify the regulatory, rather than initiating, role of JNK in programmed cell death.

Main Methods:

  • Review and synthesis of recent studies on JNK signaling and apoptosis.
  • Analysis of JNK pathway interactions with other signaling cascades, such as NF-kappaB.

Main Results:

  • JNK pathway activation acts as a "brake release" mechanism for apoptosis.
  • The JNK pathway's effect on apoptosis is context-dependent, influenced by cellular environment and stimuli.
  • Interplay with other pathways, like NF-kappaB, modulates JNK's apoptotic function.

Conclusions:

  • The JNK pathway is a crucial regulator, not an initiator, of apoptosis.
  • Understanding JNK's context-specific role is key to deciphering its function in cell death.
  • A unified model is proposed to reconcile conflicting findings on JNK and apoptosis.

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