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Updated: Nov 15, 2025

Use of Primary Cultured Hippocampal Neurons to Study the Assembly of Axon Initial Segments

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Published on: February 12, 2021

Giant ankyrin-G regulates cardiac function.

Omer Cavus¹, Jordan Williams¹, Hassan Musa¹

¹Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio, USA; The Frick Center for Heart Failure and Arrhythmia, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.

The Journal of Biological Chemistry

|March 6, 2021

Summary

This summary is machine-generated.

Giant ankyrin-G (AnkG) is crucial for heart function. Loss of giant AnkG in mice causes dilated cardiomyopathy and electrical conduction abnormalities, highlighting its vital role in cardiovascular health.

Keywords:

Nav1.5 animal model ankyrin-G arrhythmia cardiovascular disease cytoskeleton giant ankyrin-G myocytes

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

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Published on: July 5, 2021

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Cellular Electrophysiology

Background:

Cardiovascular disease (CVD) is a leading cause of death, necessitating understanding of its predisposition.
Ankyrins, particularly ankyrin-G (AnkG), are essential for membrane domain maintenance and cardiac function.
While canonical AnkG regulates cardiac excitability, the role of giant AnkG isoforms in the heart is unexplored.

Purpose of the Study:

To investigate the role of giant ankyrin-G (AnkG) in myocardial tissue.
To characterize the cardiac phenotype associated with the loss of giant AnkG in myocytes.

Main Methods:

Generation of a novel mouse model lacking giant AnkG expression specifically in myocytes (cKO).
Assessment of cardiac structure, electrical conduction, and myocyte contractility in young and adult giant AnkG cKO mice.
Transcriptomic analysis to identify molecular pathways affected by giant AnkG deficiency.

Main Results:

Giant AnkG is identified and enriched in the myocardium of young mice.
Giant AnkG cKO mice exhibit dilated cardiomyopathy, aberrant electrical conduction, and enhanced arrhythmogenicity at 1 week of age.
Loss of giant AnkG leads to delayed and early afterdepolarizations, abnormal myocyte contractility, but normal sodium current (I_Na).

Conclusions:

Giant ankyrin-G plays a critical, previously unrecognized role in maintaining cardiac structure and electrical function.
Giant AnkG deficiency results in early-onset cardiac dysfunction, suggesting its importance in neonatal and young cardiac development.
The findings reveal unique functions of giant AnkG beyond its canonical role, contributing to the diverse functions of ankyrins in the heart.