Related Experiment Videos

A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants

M Trahey1, F McCormick

  • 1Department of Molecular Biology, Cetus Corporation, Emeryville, CA 94608.

Science (New York, N.Y.)
|October 23, 1987
PubMed

Insights

Oncogenic ras p21 mutants bind guanosine triphosphate (GTP) and activate cell maturation. Normal ras p21 binds guanosine diphosphate (GDP) due to a cytoplasmic protein that enhances GTPase activity.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Ras p21 proteins are key regulators of cellular processes.
  • Guanine nucleotide binding (GTP or GDP) dictates ras p21 activity.
  • Mutations in ras p21 are implicated in oncogenesis.

Purpose of the Study:

  • To investigate the role of guanine nucleotides in ras p21 function.
  • To characterize the mechanism by which oncogenic ras p21 mutants gain activity.
  • To identify factors regulating ras p21 guanine nucleotide binding.

Main Methods:

  • Xenopus oocyte maturation assay to measure ras p21 biological activity.
  • In vivo and in vitro assays to determine ras p21 guanine nucleotide binding.
  • Biochemical analysis of cytoplasmic factors influencing ras p21 GTPase activity.

Main Results:

  • Oncogenic Asp12 and Val12 N-ras p21 mutants induced oocyte maturation, unlike normal Gly12 p21.
  • Mutant proteins were GTP-bound, while normal Gly12 p21 was GDP-bound.
  • A cytoplasmic protein significantly stimulated GTP hydrolysis by Gly12 p21, but not mutants.
  • This regulatory protein was also detected in mammalian cell extracts.

Conclusions:

  • A cytoplasmic protein maintains normal ras p21 in an inactive GDP-bound state via GTPase activity.
  • Position 12 mutations in ras p21 prevent this protein's regulatory effect, leading to an active GTP-bound state.
  • This mechanism highlights how ras p21 mutations contribute to oncogenesis by disrupting regulatory pathways.

Related Concept Videos