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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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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:
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

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Related Experiment Video

Updated: May 15, 2026

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein
07:08

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Rare codons regulate KRas oncogenesis.

Benjamin L Lampson1, Nicole L K Pershing, Joseph A Prinz

  • 1Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.

Current Biology : CB
|December 19, 2012
PubMed
Summary
This summary is machine-generated.

Differences in RAS gene codon usage impact protein expression and cancer development. Rare codons in KRAS limit its translation, unlike HRAS, affecting tumorigenic phenotypes and signaling pathways.

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Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells
09:20

Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells

Published on: July 6, 2021

Related Experiment Videos

Last Updated: May 15, 2026

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein
07:08

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells
09:20

Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells

Published on: July 6, 2021

Area of Science:

  • Molecular Biology
  • Cancer Genetics
  • Genomics

Background:

  • Oncogenic mutations in Ras GTPases (KRAS, HRAS, NRAS) lead to constitutive activation and promote cancer.
  • Ras isoforms share high sequence identity and signaling pathways, suggesting functional redundancy.
  • Despite similarities, manipulating Ras isoforms results in distinct cellular responses and tumorigenic phenotypes.

Purpose of the Study:

  • To investigate a novel regulatory mechanism explaining differential impact of Ras isoforms on tumorigenesis.
  • To elucidate how synonymous nucleotide differences in RAS genes influence protein expression and function.

Main Methods:

  • Comparative analysis of codon usage bias between KRAS and HRAS genes.
  • Experimental manipulation of rare codons to common codons in KRAS to assess expression changes.
  • Genome-wide survey to identify similar gene pairs with opposing codon bias.

Main Results:

  • KRAS exhibits poor translation compared to HRAS due to enrichment of rare codons.
  • Converting rare to common codons in KRAS significantly increases its expression and tumorigenicity.
  • Identified similar gene pairs with opposing codon bias, showing dichotomous protein expression and pathway enrichment.

Conclusions:

  • Synonymous nucleotide variations and codon usage significantly regulate KRAS and HRAS expression and function.
  • Codon bias represents a potential broader regulatory strategy in cell signaling and cancer development.