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All roads lead to FoxO

Michihiro Matsumoto1, Domenico Accili

  • 1Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.

Cell Metabolism
|August 2, 2005
PubMed

Insights

Stress-activated kinases, like c-Jun N-terminal kinase (JNK), regulate metabolism and lifespan. JNK promotes lifespan extension by phosphorylating the FoxO protein in model organisms.

Area of Science:

  • Molecular Biology
  • Genetics
  • Aging Research

Background:

  • Stress-activated kinases play a crucial role in cellular responses.
  • These kinases are known to influence metabolic pathways.
  • Insulin signaling is a key pathway regulated by stress responses.

Purpose of the Study:

  • To investigate the role of stress-activated kinases in lifespan regulation.
  • To determine the mechanism by which Jnk influences lifespan.
  • To explore the link between metabolic control, stress response, and aging.

Main Methods:

  • Studies in model organisms Drosophila and C. elegans.
  • Analysis of the phosphorylation of the forkhead protein FoxO.
  • Investigating the role of Jnk, a stress-activated kinase.

Main Results:

  • Jnk, a stress-activated kinase, was found to control lifespan in both Drosophila and C. elegans.
  • Jnk promotes lifespan extension through the phosphorylation of the FoxO protein.
  • This phosphorylation links stress responses to metabolic regulation.

Conclusions:

  • The findings establish Jnk as a key regulator of lifespan.
  • Phosphorylation of FoxO by Jnk integrates stress and metabolic signals.
  • This provides a novel mechanism connecting cellular stress responses to aging.

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