Key result
Ankyrin polypeptides play critical roles in cardiac cytoskeletal signaling, and their dysfunction is linked to inherited and acquired arrhythmias including long-QT syndrome and atrial fibrillation.
Ankyrin polypeptides are critical for cardiac ion channel targeting and regulation, and their dysfunction is linked to a broad spectrum of inherited and acquired arrhythmias.
Ankyrin evaluation may inform select arrhythmia cases; leaves open targeted therapy development pending further study.
Ankyrin polypeptides are cellular adapter proteins that tether integral membrane proteins to the cytoskeleton in a host of human organs. Initially identified as integral components of the cytoskeleton in erythrocytes, a recent explosion in ankyrin research has demonstrated that these proteins play prominent roles in cytoskeletal signaling pathways and membrane protein trafficking/regulation in a variety of excitable and non-excitable cells including heart and brain. Importantly, ankyrin research has translated from bench to bedside with the discovery of human gene variants associated with ventricular arrhythmias that alter ankyrin-based pathways. Ankyrin polypeptides have also been found to play an instrumental role in various forms of sinus node disease and atrial fibrillation (AF). Mouse models of ankyrin-deficiency have played fundamental roles in the translation of ankyrin-based research to new clinical understanding of human sinus node disease, AF, and ventricular tachycardia.
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Smith et al. (2012) conducted a review in Arrhythmia and sudden cardiac death. Ankyrin dysfunction was evaluated. Ankyrin polypeptides play critical roles in cardiac cytoskeletal signaling, and their dysfunction is linked to inherited and acquired arrhythmias including long-QT syndrome and atrial fibrillation.
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