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In-vitro Mutagenesis

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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Related Experiment Video

Updated: May 17, 2026

Targeted Knockdown of Genes in the Choroid Plexus

Targeted Knockdown of Genes in the Choroid Plexus

Published on: June 16, 2023

Producing PPARgamma2 knockdown in mouse liver.

Tomomi Yamazaki¹, Osamu Ezaki

¹Nutritional Science Program, National Institute of Health and Nutrition, Tokyo, Japan. tomo0322@nih.go.jo

Methods in Molecular Biology (Clifton, N.J.)

|October 27, 2012

Summary

High saturated fat diets cause fatty liver by increasing PPARγ2 protein. Inactivating PPARγ2 (peroxisome proliferator-activated receptor gamma 2) may treat this condition, offering a therapeutic target.

Area of Science:

Hepatology
Molecular Biology
Metabolic Diseases

Background:

High saturated fat intake is a known cause of non-alcoholic fatty liver disease (NAFLD).
The peroxisome proliferator-activated receptor gamma 2 (PPARγ2) is implicated in regulating lipid metabolism and may play a role in NAFLD pathogenesis.
Increased PPARγ2 expression correlates with the development of fatty liver.

Purpose of the Study:

To investigate the role of PPARγ2 in diet-induced fatty liver.
To develop a method for PPARγ2 inactivation using RNA interference (RNAi) for therapeutic and research purposes.

Main Methods:

Construction of an adenovirus vector carrying short hairpin RNA (shRNA) targeting PPARγ2.
Utilizing adenovirus vector-mediated RNAi to reduce PPARγ2 expression in a mouse model of diet-induced fatty liver.

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Main Results:

The study describes the successful construction of an adenovirus vector for PPARγ2 RNAi.
This method is proposed as a tool to elucidate the biological role of PPARγ2 in various tissues and diseases.

Conclusions:

PPARγ2 is a key mediator in the development of fatty liver induced by high saturated fat diets.
Adenovirus-mediated RNA interference of PPARγ2 is a promising strategy for both understanding its role and for potential therapeutic interventions in fatty liver disease and other metabolic disorders.