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Inhibition by cAMP of Ras-dependent activation of Raf

S J Cook1, F McCormick

  • 1Onyx Pharmaceuticals, Richmond, CA 94806.

Science (New York, N.Y.)
|November 12, 1993
PubMed

Insights

Elevated cyclic adenosine 3

Area of Science:

  • Cellular signaling pathways
  • Molecular biology
  • Signal transduction

Background:

  • Mitogenic signaling involves Raf and extracellular signal-regulated kinases (ERKs).
  • Interactions between mitogenic signaling and other pathways remain largely uncharacterized.

Purpose of the Study:

  • To investigate the inhibitory effects of cyclic adenosine 3',5'-monophosphate (cAMP) on mitogenic signaling pathways.
  • To elucidate the specific mechanisms by which cAMP interferes with signal transduction.

Main Methods:

  • Utilized Rat1 cells treated with epidermal growth factor (EGF) or lysophosphatidic acid.
  • Assessed the impact of elevated intracellular cAMP levels on DNA synthesis and signal transduction.
  • Analyzed receptor tyrosine kinase activity, Grb2/Shc association, Ras-GTP levels, and Raf-1/ERK activation.

Main Results:

  • Elevated cAMP blocked DNA synthesis and signal transduction induced by EGF and lysophosphatidic acid.
  • cAMP did not affect EGF receptor tyrosine kinase activity or its association with Grb2 and Shc.
  • cAMP did not alter EGF-dependent Ras-GTP accumulation but inhibited Raf-1 and ERK activation.

Conclusions:

  • Cyclic adenosine 3',5'-monophosphate (cAMP) inhibits signal transmission from Ras to Raf-1.
  • cAMP prevents Ras-dependent activation of Raf-1, thereby blocking downstream ERK activation.
  • This study reveals a novel inhibitory role of cAMP in the Ras-Raf-ERK signaling cascade.

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