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Generation and Characterization of Smad7 Conditional Knockout Mice
1Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Abstract:
Smad7 is an important negative modulator that regulates the duration and strength of TGF-β signaling. Dysregulation of Smad7 is associated with the pathogenesis of many human diseases. Various mouse models are developed to facilitate addressing the physiological functions of Smad7. We have recently demonstrated that loss of Smad7 function by deletion in its MH2 domain leads to multiple cardiac defects and aggravates ethanol-induced liver injury. Here, we describe the procedure to construct and characterize the Smad7 conditional knockout mice.
Insights
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.
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.
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