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Related Concept Videos

The Ras Gene02:38

The Ras Gene

6.5K
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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Mutations in Microorganisms01:18

Mutations in Microorganisms

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Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
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Mutations01:39

Mutations

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Overview
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In-vitro Mutagenesis01:16

In-vitro Mutagenesis

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To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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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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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Related Experiment Video

Updated: Oct 1, 2025

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

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A mutation breaks its silence on mutant KRAS.

Amy E Baek1

  • 1Science Signaling, AAAS, Washington, DC 20005, USA.

Science Signaling
|March 8, 2022
PubMed
Summary

This study shows how silent mutations and alternative splicing can be used to target KRAS mutant cells. These genetic mechanisms offer new strategies for cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • KRAS mutations are common drivers in many cancers, presenting a significant therapeutic challenge.
  • Targeting KRAS directly has historically been difficult due to its intracellular localization and lack of effective inhibitors.
  • Alternative splicing and silent mutations represent underutilized areas for therapeutic intervention.

Purpose of the Study:

  • To investigate the potential of exploiting silent mutations and alternative splicing events to specifically target KRAS-mutant cancer cells.
  • To develop novel therapeutic strategies that leverage these genetic alterations for improved cancer treatment.

Main Methods:

  • Analysis of genomic and transcriptomic data from KRAS-mutant cancer cohorts.
  • In silico prediction and validation of alternative splicing events associated with KRAS mutations.

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  • Development and application of molecular tools to target specific splice variants or exploit silent mutations.

    • Main Results:

    • Identification of specific alternative splicing events that are uniquely present or altered in KRAS-mutant tumors.
    • Demonstration that silent mutations can influence KRAS protein function or cellular response.
    • Validation of strategies to selectively target KRAS-mutant cells based on identified splicing patterns or silent mutation contexts.

    Conclusions:

    • Silent mutations and alternative splicing provide novel avenues for developing targeted therapies against KRAS-driven cancers.
    • Exploiting these genetic mechanisms offers a promising approach to overcome resistance and improve treatment efficacy for KRAS-mutant malignancies.