The findings, published in the Proceedings of the National Academy of Sciences, detail how PIP2 plays a crucial role in regulating the SK2 channel.

PIP2 is essential for various signaling pathways and is known to be dysregulated in heart failure, which could contribute to cardiac arrhythmias.

The insights gained from this study could pave the way for developing novel SK2 channel inhibitors for treating cardiac arrhythmias.

The collaboration among researchers is ongoing, with plans to study other SK channel subtypes and explore drug modulation for prospective AFib treatments.

This study is timely, as SK channel inhibitors are currently undergoing clinical trials for AFib treatment.

The research utilized innovative experimental and computational methods to understand how the human SK2 channel is dynamically co-regulated.

Researchers from the University of Arizona College of Medicine–Phoenix and UC Davis Health have identified a new target for treating atrial fibrillation (AFib), the most common type of abnormal heart rhythm.

AFib is responsible for approximately 1 in 7 strokes and significantly increases the risk of morbidity and mortality, with projections indicating that over 12 million people will be affected by 2030.

Current treatments for AFib are considered inadequate, prompting ongoing research into more effective therapies.

The study focuses on small-conductance calcium-activated potassium channels (SK channels), particularly the SK2 channel, which has been a longstanding research target for AFib treatment.

SK channels are currently the only potassium channels known to be upregulated in heart failure, making their regulation essential for understanding arrhythmias.

The research team created models of the SK2 channel in various states and utilized molecular dynamics simulations to explore how the lipid phosphatidylinositol 4,5-bisphosphate (PIP2) modulates its function.