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Related Experiment Videos

Ras versus cyclin-dependent kinase inhibitors

A C Lloyd1

  • 1MRC Laboratory for Molecular Cell Biology, University College London, London, UK. alison.lloyd@ucl.ac.uk

Current Opinion in Genetics & Development
|April 8, 1998
PubMed
Summary

Activated Ras protein can halt cell division in primary cells by inducing cell-cycle inhibitors. However, in immortalized cells lacking Ras signals, Ras promotes cell cycle progression, with new insights into how it overrides controls.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Ras proteins are key regulators of cell signaling pathways.
  • Cell cycle progression is tightly controlled by various regulatory proteins.
  • Dysregulation of Ras signaling and cell cycle control is implicated in cancer development.

Purpose of the Study:

  • To elucidate the complex interactions between Ras signaling and cell cycle regulation.
  • To understand how Ras influences cell cycle arrest in primary cells.
  • To investigate the mechanisms by which Ras promotes cell cycle progression in immortalized cells.

Main Methods:

  • Analysis of Ras protein activity in different cell types.
  • Investigation of cyclin-dependent kinase inhibitor (CDKI) expression and function.

Related Experiment Videos

  • Studies on oncogenic mutations cooperating with Ras.
  • Examination of cell cycle control mechanisms in Ras-altered cells.

    • Main Results:

    • Activated Ras induces cell-cycle arrest in primary cells through CDKIs.
    • Oncogenic alterations cooperate with Ras by neutralizing CDKIs.
    • In immortalized cells lacking negative Ras growth signals, Ras promotes cell cycle progression.
    • Mechanisms by which Ras overrides cell cycle checkpoints have been identified.

    Conclusions:

    • Ras plays a dual role in cell cycle regulation depending on cellular context.
    • Understanding Ras-cell cycle interactions is crucial for cancer research.
    • Targeting Ras pathways offers potential therapeutic strategies for cancers driven by Ras dysregulation.