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Related Experiment Videos

Normal and transforming Ras are differently regulated for posttranslational modifications

T Yamada-Okabe1, R Doi, H Yamada-Okabe

  • 1Department of Hygiene, Yokohama City University, School of Medicine Japan.

Journal of Cellular Biochemistry
|May 1, 1996
PubMed
Summary

Point mutations in the c-H-ras gene enhance Ras transforming activity. While both normal and mutated Ras localize to membranes, the mutated form does so more efficiently, but c-myc oncogene co-expression inhibits this process.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Biology

Background:

  • Ras proteins are crucial for cell signaling and transformation.
  • Posttranslational modification and membrane localization are essential for Ras biological activity.
  • Point mutations in the c-H-ras gene can lead to increased cellular transforming activities.

Purpose of the Study:

  • To investigate how c-H-ras gene mutations affect Ras posttranslational modification and membrane localization.
  • To compare the processing of normal (Gly12) versus transforming (Val12) Ras.
  • To determine the impact of co-expressed oncogenes (c-myc, p53) on Ras modification and localization.

Main Methods:

  • Expression of normal and mutant c-H-ras genes in NIH3T3 cells using a metallothionein promoter.

Related Experiment Videos

  • Induction of gene expression with cadmium treatment.
  • Immunoprecipitation of metabolically labeled cell extracts.
  • Analysis of Ras forms by SDS-polyacrylamide gel electrophoresis.

    • Main Results:

    • Both normal and transforming Ras were expressed and localized to the membrane.
    • Transforming Ras exhibited more efficient processing and membrane-bound forms compared to normal Ras.
    • Co-expression of the c-myc oncogene significantly inhibited Ras posttranslational modification and membrane localization.
    • Expression of p53 (wild type or mutant) did not affect Ras modification or localization.

    Conclusions:

    • Ras point mutations enhance membrane localization, contributing to increased transforming activity.
    • The c-myc oncogene specifically interferes with Ras posttranslational modification and membrane targeting.
    • These findings highlight a potential mechanism by which c-myc cooperates with Ras in oncogenesis.