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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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...
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Small GTPases - Ras and Rho01:24

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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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Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
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Functional distinction in oncogenic Ras variant activity in Caenorhabditis elegans.

Haimeng Lyu1, Helen M Chamberlin1

  • 1Department of Molecular Genetics, Ohio State University, 484 West 12th Avenue, Columbus, OH 43210, USA.

Disease Models & Mechanisms
|July 1, 2024
PubMed
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Oncogenic Ras variants, crucial in cancer, show distinct behaviors within cellular networks. This study reveals how different Ras mutations impact development and drug responses in vivo.

Keywords:
C. elegans vulva developmentOncogenic Ras variantsRas/MEK signaling pathway

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Area of Science:

  • Oncology
  • Molecular Biology
  • Developmental Biology

Background:

  • Ras genes are key oncogenes frequently mutated in human cancers.
  • Distinct oncogenic Ras variants have varied effects on cancer types, cellular targets, and drug sensitivity.
  • Understanding how these variants interact with cellular networks is crucial but poorly understood.

Purpose of the Study:

  • To identify novel components in the interplay between Ras genotype and cellular interaction networks in vivo.
  • To investigate the functional distinctions of specific Ras oncogenic substitution changes.
  • To explore how different Ras variants respond to genetic modulators and extracellular signals.

Main Methods:

  • Development and application of a vulva-development assay in the nematode C. elegans as an experimental framework.
  • Evaluation of Ras oncogenic substitution changes at G12, G13, and Q61.
  • Analysis of phenotypic differences, sensitivity to gene dosage, and MEK inhibition.

Main Results:

  • Ras oncogenic variants were categorized into distinct groups based on observed phenotypic differences.
  • Variant responses varied concerning gene dosage sensitivity and inhibition of the downstream kinase MEK.
  • Genetic modulators influencing Ras activity non-autonomously demonstrated variant-restricted effects in vivo.

Conclusions:

  • Oncogenic Ras variants in C. elegans display distinct mechanisms of interaction with the vulva-development network.
  • Extracellular modulators exert variant-specific effects on Ras activity and downstream pathways in vivo.
  • This study provides a framework for dissecting Ras variant functions in a complex biological network.