Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

The Ras Gene

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...

Mutations

Mutations

Mutations

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

One-Way ANOVA: Equal Sample Sizes

One-Way ANOVA: Equal Sample Sizes

One-Way ANOVA can be performed on three or more samples with equal or unequal sample sizes. When one-way ANOVA is performed on two datasets with samples of equal sizes, it can be easily observed that the computed F statistic is highly sensitive to the sample mean.
Different sample means can result in different values for the variance estimate: variance between samples. This is because the variance between samples is calculated as the product of the sample size and the variance between the...

Small GTPases - Ras and Rho

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:

Viral Mutations

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition.

Cell reports·2026

Same author

Advances in RAS Therapeutics for Pancreatic Cancer.

The New England journal of medicine·2026

Same author

Characterization and therapeutic suppression of KEAP1-NRF2-driven resistance to KRAS inhibitors in pancreatic and lung cancer.

bioRxiv : the preprint server for biology·2026

Same author

KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Pancreatic Cancer.

Cancer research·2026

Same author

Dordaviprone/ONC201 Activation of the ClpP Mitochondrial Protease Inhibits the Growth of KRAS-Mutant Pancreatic Cancer and Overcomes RAS Inhibitor Resistance.

bioRxiv : the preprint server for biology·2026

Same author

KRASG12R-Mutant Pancreatic Cancer Features Limited ERK/MAPK Transcriptional Activity and a Distinctive Tumor Microenvironment.

Cancer research·2026

Search research articles

Related Experiment Video

Updated: Jan 24, 2026

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

RAS Mutations Are Not Created Equal.

G Aaron Hobbs¹, Channing J Der^2,3

¹Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

Cancer Discovery

|June 5, 2019

Summary

This summary is machine-generated.

Specific KRAS mutations, like G12D and A146T, cause distinct structural changes and tissue-specific effects. Understanding these differences is key for developing targeted cancer therapies.

More Related Videos

Demonstration of Equal-Intensity Beam Generation by Dielectric Metasurfaces

Demonstration of Equal-Intensity Beam Generation by Dielectric Metasurfaces

Published on: June 7, 2019

How to Create and Use Binocular Rivalry

How to Create and Use Binocular Rivalry

Published on: November 10, 2010

Related Experiment Videos

Last Updated: Jan 24, 2026

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Demonstration of Equal-Intensity Beam Generation by Dielectric Metasurfaces

Demonstration of Equal-Intensity Beam Generation by Dielectric Metasurfaces

Published on: June 7, 2019

How to Create and Use Binocular Rivalry

How to Create and Use Binocular Rivalry

Published on: November 10, 2010

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

KRAS is a frequently mutated oncogene in human cancers.
Different KRAS mutations can lead to varied clinical outcomes.
Understanding mutation-specific effects is crucial for targeted cancer therapy.

Purpose of the Study:

To investigate the structural, biochemical, and biological consequences of two distinct KRAS mutations (G12D and A146T).
To determine if KRAS mutations have tissue-specific signaling and biological impacts.

Main Methods:

Structural analysis of KRAS mutants.
Biochemical assays to assess KRAS function.
Biological profiling in relevant cancer models.

Main Results:

KRAS G12D and A146T mutations exhibit distinct structural and biochemical profiles.
The same KRAS mutation can lead to different signaling pathways and biological effects depending on the tissue type.
These findings highlight the heterogeneity of KRAS-driven cancers.

Conclusions:

KRAS mutation type dictates specific structural and functional alterations.
Tissue context significantly influences the biological consequences of KRAS mutations.
This research provides a foundation for developing mutation- and tissue-specific KRAS-targeted therapies.