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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Transcription-dependent and -independent control of neuronal survival by the PI3K-Akt signaling pathway

A Brunet1, S R Datta, M E Greenberg

  • 1Division of Neuroscience, Children's Hospital and Department of Neurology, Harvard Medical School, Boston, MA 02115, USA. brunet_a@a1.tch.harvard.edu

Current Opinion in Neurobiology
|June 12, 2001
PubMed

Insights

The PI3K-Akt pathway is crucial for neuron survival, blocking cell death through various mechanisms. Akt regulates both the cell death machinery and gene expression, potentially influencing metabolic pathways for survival.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • The Phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway is vital for neuronal survival.
  • Akt, a serine/threonine kinase, has identified substrates involved in cell death regulation.

Purpose of the Study:

  • To elucidate the multifaceted roles of the PI3K-Akt pathway in neuronal cell survival.
  • To explore how Akt modulates cell death machinery and gene expression.
  • To investigate the potential involvement of metabolic pathways in Akt-mediated survival.

Main Methods:

  • This study focuses on the known functions and substrates of Akt.
  • It reviews recent experimental findings on Akt's role in cell death and survival.
  • The review incorporates evidence on Akt's interaction with metabolic pathways.

Main Results:

  • Akt inhibits neuronal cell death by affecting cytoplasmic death mechanisms.
  • Akt regulates the expression of genes critical for cell death and survival.
  • Emerging evidence indicates Akt influences cell survival through metabolic regulation.

Conclusions:

  • The PI3K-Akt pathway is a key regulator of neuronal survival through diverse mechanisms.
  • Akt's actions extend to cytoplasmic pathways, gene expression, and metabolic processes.
  • Further research into Akt's metabolic roles could reveal new therapeutic targets for neuronal survival.

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