Journal
/
Genética
/
Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
JoVE Revista
Genética
Se requiere una suscripción a JoVE para ver este contenido.  Inicie sesión o comience su prueba gratuita.
JoVE Revista Genética
Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

DOI:
10.3791/63949-v

•

03:45 min

•

August 08, 2022

•

, , , , , , , , ,
1Department of Cardiovascular Surgery, Guangdong Provincial Hospital of Traditional Chinese Medicine,the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, 2The Second Clinical College of Guangzhou University of Chinese Medicine, 3Department of Cardiovascular Surgery, The First Affiliated Hospital,Jinan University, 4Guangdong Provincial Key Laboratory of Laboratory Animals,Guangdong Laboratory Animals Monitoring Institute, 5Department of Anesthesiology, Guangdong Provincial Hospital of Chinese Medicine,the Second Affiliated Hospital of Guangzhou University of Chinese Medicine

Capítulos

  • 00:04Introduction
  • 00:35Evaluation of the Cardiac Morphology and Function
  • 01:54Results: Validating the Pathogenicity of G823E Mutation Using the C57BL/6N Murine Model
  • 03:17Conclusion

Summary

Traducción Automática

Traducción Automática

Based on the familial hereditary cardiomyopathy family found in our clinical work, we created a C57BL/6N mouse model with a point mutation (G823E) at the mouse MYH7 locus through CRISPR/Cas9-mediated genome engineering to verify this mutation.

Tags

Familial Hypertrophic CardiomyopathyMYH7 MutationGly823GluMouse ModelUltrasoundEchocardiographyCardiac HypertrophySanger SequencingGenetic Etiology

Article

Embed

Añadir a la lista de reproducción

Usage Statistics

Videos relacionados

Detection of Copy Number Alterations Using Single Cell Sequencing

A Standard Methodology to Examine On-site Mutagenicity As a Function of Point Mutation Repair Catalyzed by CRISPR/Cas9 and SsODN in Human Cells

Efficient Production and Identification of CRISPR/Cas9-generated Gene Knockouts in the Model System Danio rerio

Profiling DNA Replication Timing Using Zebrafish as an In Vivo Model System

Using Mouse Oocytes to Assess Human Gene Function During Meiosis I

Visualization of Microbiota in Tick Guts by Whole-mount In Situ Hybridization

Exploring the Effects of Spaceflight on Mouse Physiology using the Open Access NASA GeneLab Platform

Using In Vitro and In-cell SHAPE to Investigate Small Molecule Induced Pre-mRNA Structural Changes

Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models

Determining the Egg Fertilization Rate of Bemisia tabaci Using a Cytogenetic Technique

Read Article