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Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:

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Related Experiment Video

Updated: Jun 5, 2026

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

Compartmentalized Ras proteins transform NIH 3T3 cells with different efficiencies.

Chiang-Min Cheng1, Huiling Li, Stéphane Gasman

  • 1Department of Molecular and Cellular Biology, Lester and Sue Smith Breast Center, 1 Baylor Plaza, Baylor College of Medicine, Houston, TX 77030, USA.

Molecular and Cellular Biology
|December 30, 2010
PubMed
Summary
This summary is machine-generated.

Oncogenic Ras proteins transform cells by interacting with Cdc42 on the endomembrane. This interaction is crucial for Ras GTPases to fully transform cells, requiring cooperative action from multiple compartment-specific pathways.

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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
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Inducible and Reversible Dominant-negative (DN) Protein Inhibition
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Inducible and Reversible Dominant-negative (DN) Protein Inhibition

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Last Updated: Jun 5, 2026

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

Inducible and Reversible Dominant-negative (DN) Protein Inhibition
08:35

Inducible and Reversible Dominant-negative (DN) Protein Inhibition

Published on: January 7, 2019

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Ras GTPases were traditionally considered to function solely from the plasma membrane (PM).
  • Emerging models propose Ras protein compartmentalization for distinct regulatory functions.
  • Oncogenic H-Ras mutants restricted to the endomembrane retain transforming capabilities.

Purpose of the Study:

  • To investigate the role of endomembrane-localized Ras proteins in cell transformation.
  • To identify downstream targets of endomembrane Ras pathways.
  • To elucidate the cooperative mechanisms between Ras and Cdc42 in cell transformation.

Main Methods:

  • Tumor formation assays in nude mice using endomembrane-restricted H-Ras.
  • Analysis of Cdc42 activity in response to endomembrane-restricted H-Ras.
  • Co-immunoprecipitation to detect H-Ras/Cdc42 complex formation on the endomembrane.
  • Cell transformation assays with PM-restricted H-Ras and coexpressed Cdc42.

Main Results:

  • Endomembrane-restricted oncogenic H-Ras induced tumor formation.
  • Inhibition of Cdc42 activity blocked H-Ras-induced cell transformation.
  • H-Ras formed a complex with Cdc42 on the endomembrane, with enhanced interaction upon GTP binding or growth factor stimulation.
  • PM-restricted H-Ras activated Raf-1 and induced senescence but showed weak transformation alone, which was enhanced by coexpressed Cdc42.

Conclusions:

  • Efficient cell transformation necessitates Ras interaction with Cdc42 on the endomembrane.
  • Cooperative signaling between compartment-specific Ras pathways is essential for full cellular transformation.
  • Endomembrane Ras-Cdc42 signaling is a critical pathway for oncogenesis.