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Generation of Brown Fat-Specific Knockout Mice Using a Combined Cre-LoxP, CRISPR-Cas9, and Adeno-Associated Virus Single-Guide RNA System

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Generation and Characterization of Smad7 Conditional Knockout Mice.

Yi Pan¹, Yan Chen²

¹Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.

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

|November 2, 2015

Summary

Smad7 protein is crucial for regulating TGF-β signaling. We created Smad7 conditional knockout mice to study its role in diseases, revealing its importance in cardiac and liver health.

Keywords:

Gene deletion Heart development Mouse model Smad7

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

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Area of Science:

Molecular Biology
Genetics
Physiology

Background:

Smad7 acts as a key negative regulator of Transforming Growth Factor-beta (TGF-β) signaling pathways.
Altered Smad7 expression and function are implicated in the development of various human diseases.
Understanding Smad7's physiological roles is essential for disease research.

Purpose of the Study:

To describe the methodology for generating and validating Smad7 conditional knockout (cKO) mouse models.
To provide a tool for investigating the in vivo functions of Smad7.

Main Methods:

Construction of Smad7 conditional knockout mouse lines.
Characterization of the generated mouse models.
Phenotypic analysis of Smad7 loss-of-function.

Main Results:

Successful generation of Smad7 cKO mice.
Demonstrated that Smad7 loss-of-function causes cardiac abnormalities.
Observed exacerbation of ethanol-induced liver injury in Smad7-deficient mice.

Conclusions:

Smad7 plays a critical role in maintaining cardiac and liver homeostasis.
Smad7 cKO mice are valuable models for studying TGF-β signaling and related pathologies.
Further research using these models can elucidate Smad7's contribution to human diseases.