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In-vitro Mutagenesis

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: Jun 11, 2026

Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish

Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish

Published on: July 22, 2025

Generation of Fgfr3 conditional knockout mice.

Nan Su¹, Xiaoling Xu, Cuiling Li

¹State Key Laboratory of Trauma, Burns and Combined Injury, Center of Bone Metabolism and Repair, Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China.

International Journal of Biological Sciences

|June 29, 2010

Summary

This summary is machine-generated.

Researchers developed conditional knockout mice to study Fibroblast Growth Factor Receptor 3 (FGFR3) roles in development and disease. This model allows targeted gene deletion in cartilage, aiding research into FGFR3-related conditions.

Keywords:

Cre-Loxp FGFR3 conditional knock out gene targeting

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

Molecular Biology
Developmental Biology
Genetics

Background:

Fibroblast Growth Factor Receptor 3 (FGFR3) is a crucial tyrosine kinase receptor involved in various developmental processes.
FGFR3 mutations are linked to human skeletal disorders like achondroplasia (ACH), hypochondroplasia (HCH), and thanatophoric dysplasia (TD).
Conventional Fgfr3 knockout models exhibit severe phenotypes, limiting detailed study of its tissue-specific functions.

Purpose of the Study:

To create a conditional knockout mouse model for investigating the specific roles of FGFR3 in different tissues and developmental stages.
To enable precise deletion of Fgfr3 alleles in cartilage using Cre-lox technology.

Main Methods:

Generation of Fgfr3 conditional knockout mice with loxp sites flanking exons 9-10.
Utilizing Cre-mediated recombination with Col2a1-Cre to achieve chondrocyte-specific deletion of Fgfr3.
Characterization of the resulting animal model for studying FGFR3 function.

Main Results:

Successfully generated Fgfr3 conditional knockout mice.
Demonstrated effective, cartilage-specific gene deletion using Col2a1-Cre.
Established a valuable tool for dissecting FGFR3's diverse roles.

Conclusions:

The developed Fgfr3 conditional knockout mouse model provides a powerful platform for studying FGFR3 function.
This model facilitates research into the complex roles of FGFR3 in skeletal development and related pathologies.
Future studies can utilize this model to elucidate tissue-specific functions and therapeutic targets for FGFR3-associated diseases.