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GTP-binding proteins and adenylate cyclase activity in v-Ki-ras transformed NIH/3T3 fibroblast cells

L Konishi-Imamura1, M Tohda, M Noda

  • 1Department of Pharmacology, Toyama Medical and Pharmaceutical University, Japan.

Insights

Ras oncogene p21 enhances GTP-binding protein coupling to adenylate cyclase. v-Ki-ras transformation decreases inhibitory Gi protein, enhancing Gs-mediated stimulation.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Oncology

Background:

  • Ras oncogene and p21 are implicated in cellular signaling pathways.
  • Previous studies showed enhanced adenylate cyclase activity in ras-transformed cells.
  • GTP-binding proteins (G proteins) regulate adenylate cyclase activity.

Purpose of the Study:

  • To elucidate the role of ras oncogene and p21 in G protein-adenylate cyclase coupling.
  • To investigate the impact of v-Ki-ras transformation on G protein levels and activity.

Main Methods:

  • Utilized v-Ki-ras transformed NIH/3T3 fibroblast cells and normal NIH/3T3 cells.
  • Assessed adenylate cyclase activity using GTP gamma S.
  • Quantified G protein levels (Gs and Gi) via [32P] ADP-ribosylation assays with cholera toxin and pertussis toxin.

Main Results:

  • GTP gamma S more significantly enhanced adenylate cyclase in transformed cells.
  • Gs protein levels were comparable between normal and transformed cells.
  • Gi protein levels were reduced by approximately one-third in v-Ki-ras transformed cells compared to normal cells.

Conclusions:

  • p21 associated with ras oncogene likely enhances the coupling of GTP-binding proteins to adenylate cyclase.
  • v-Ki-ras transformation leads to decreased Gi protein levels.
  • Reduced Gi protein results in diminished inhibitory regulation of adenylate cyclase, enhancing the stimulatory influence of Gs.

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