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Insulin-stimulated MAP-2 kinase phosphorylates and activates ribosomal protein S6 kinase II

T W Sturgill1, L B Ray, E Erikson

  • 1Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville 22903.

Nature
|August 25, 1988
PubMed

Insights

Insulin signaling involves sequential activation of protein kinases. Phosphorylation of ribosomal protein S6 and S6 kinase II by other kinases suggests a cascade in cellular growth regulation.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Biochemistry

Background:

  • Ribosomal protein S6 is a key component of the eukaryotic 40S ribosomal subunit.
  • S6 phosphorylation occurs in response to mitogens like insulin, growth factors, and viral oncoproteins.
  • Understanding the regulation of S6 phosphorylation is crucial for deciphering cellular growth and proliferation pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying insulin signaling.
  • To characterize the activated S6 kinase II (S6 K II) purified from Xenopus eggs.
  • To explore the sequential activation of protein kinases involved in insulin signal transduction.

Main Methods:

  • Purification of activated S6 kinase II (S6 K II) from Xenopus eggs.
  • In vitro deactivation assays using protein phosphatase 1 and protein phosphatase 2A.
  • In vitro reactivation and phosphorylation studies using an insulin-stimulated MAP-2 protein kinase.

Main Results:

  • Purified S6 K II can be deactivated by protein phosphatase 1 or 2A.
  • S6 K II reactivation and phosphorylation in vitro involves an insulin-stimulated MAP-2 protein kinase.
  • The MAP-2 protein kinase is itself a phosphoprotein regulated by protein phosphatase 2A.

Conclusions:

  • Insulin signaling appears to involve a sequential activation cascade of at least two serine/threonine protein kinases.
  • This cascade culminates in the phosphorylation of S6 kinase II and subsequently ribosomal protein S6.
  • The findings provide insights into the intricate regulation of protein kinases in response to growth factor signaling.

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