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Related Experiment Video

Updated: Feb 10, 2026

Improved Genome Editing via Oviductal Nucleic Acids Delivery-based In Vivo Electroporation Technique for Knockout Mice Generation

Improved Genome Editing via Oviductal Nucleic Acids Delivery-based In Vivo Electroporation Technique for Knockout Mice Generation

Published on: August 26, 2025

Generation of Smurf2 Conditional Knockout Mice.

Yi Tang¹, Liu-Ya Tang¹, Xuan Xu¹

¹Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

International Journal of Biological Sciences

|May 29, 2018

Summary

This summary is machine-generated.

Smad ubiquitin regulatory factor 2 (Smurf2) is crucial for development. Researchers created conditional Smurf2 knockout mice to study its roles in adult tissues, enabling new insights into its functions.

Keywords:

Knockout Liver LoxP Mice Smurf2

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Last Updated: Feb 10, 2026

Improved Genome Editing via Oviductal Nucleic Acids Delivery-based In Vivo Electroporation Technique for Knockout Mice Generation

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Generating Transgenics and Knockouts in Strongyloides Species by Microinjection

Generating Transgenics and Knockouts in Strongyloides Species by Microinjection

Published on: October 7, 2021

Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

Smad ubiquitin regulatory factor 2 (Smurf2) is an E3 ubiquitin ligase.
Initially known as a negative regulator of TGF-β and BMP signaling, Smurf2's functions extend to genomic stability, cell polarity, and carcinogenesis.
Conventional Smurf1/Smurf2 double knockout mice exhibit embryonic lethality, necessitating models for studying Smurf2 in later development.

Purpose of the Study:

To generate a conditional Smurf2 knockout mouse model for investigating its physiological functions in specific tissues and ages.
To validate the efficacy of Cre-mediated recombination for targeted Smurf2 gene inactivation.

Main Methods:

Generation of Smurf2 conditional knockout mice.
Utilizing Cre-loxP system for targeted gene deletion.
Employing Alb-Cre for liver-specific deletion and generating Smurf2 knockout MEFs.

Main Results:

Cre-mediated recombination with Alb-Cre successfully deleted the Smurf2 gene in liver tissue.
Smurf2 deficiency in mouse embryonic fibroblasts (MEFs) was confirmed, impacting multiple signaling pathways.
The developed animal model allows for tissue-specific and age-dependent studies of Smurf2.

Conclusions:

Conditional Smurf2 knockout mice provide a valuable tool for studying Smurf2's diverse roles in various tissues and developmental stages.
This model overcomes the limitations of embryonic lethality in conventional knockouts.
Further research using this model will elucidate Smurf2's specific contributions to tissue homeostasis and disease.