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New Loyola study on IKs channels in the heart published in PNAS

The slow potassium channel in the heart, IKs, responds to sympathetic nervous system (the body’s ‘fight or flight’ response) to adjust the time the ventricles have to fill with blood in response to changes in heart rate. These channels open to allow potassium ions to pass out of cells, relaxing the heart muscle to its resting state at the end of each beat.

In a new study in Proceedings of the National Academy of Sciences (PNAS), Steve Goldstein, MD, PhD, dean of the Stritch School of Medicine, and professor in the departments of pediatrics and cell and molecular physiology led a team comprised of Drs. Dazhi Xiong and Hui Dai, also in the department of cell and molecular physiology, and former colleagues at Brandeis University, showing that the energy it takes to open IKs channels depends on the number of times they are modified by small ubiquitin-like modifier (SUMO) proteins.

The exquisite and adjustable sensitivity of IKs channels is what makes them so important to the length and rhythm of cardiac action potentials. During a cardiac action potential there is a brief positive change in the voltage across a heart cell’s membrane, which leads the heart to contract and pump blood and also opens IKs channel after a delay to end the heartbeat. The work shows that SUMO is central to how IKs channels operate.

IKs channels can be modified by SUMO up to four times and each SUMO shifts the increase in voltage required to open the channels. Whereas ubiquitin modification controls protein half-life, SUMO controls protein function.

The funding for this research was provided by the National Heart, Lung and Blood Institute. The full paper can found on the PNAS website.