New view of the heartbeat

The human cardiac voltage-gated sodium channel (Nav1.5) plays a critical role in maintaining regular heartbeats. Mutations in Nav1.5 cause life-threatening heart rhythm disorders (arrhythmias).

Nav1.5 is sensitive to the calcium-ion sensor protein calmodulin (CaM); however, the exact mechanism of how CaM exerts its effect on Nav1.5 is not well understood.

In a study published in the journal Structure, Christopher Johnson, Ph.D., Walter Chazin, Ph.D., and their colleagues integrated structural biology data from multiple techniques to show that CaM engages a portion of Nav1.5 known as the "inactivation gate" in a unique manner.

Then they determined that this calcium-dependent binding of CaM promotes the resetting of the after it opens, to help prepare for the next heartbeat.

Their work suggests a mechanism for how calcium and calmodulin fine tune cardiac sodium channels and may help in the development of novel therapeutics and improvements to existing treatments for .

More information: Christopher N. Johnson et al. A Mechanism of Calmodulin Modulation of the Human Cardiac Sodium Channel, Structure (2018). DOI: 10.1016/j.str.2018.03.005

Journal information: Structure
Citation: New view of the heartbeat (2018, April 9) retrieved 21 February 2024 from https://medicalxpress.com/news/2018-04-view-heartbeat.html
This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.

Explore further

Leaky channels could contribute to unusual heart arrhythmias

3 shares

Feedback to editors