Potassium channel subfamily K member 3 (KCNK3) (K2P3.1)

Potassium channel subfamily K member 3 (KCNK3), also known as TASK-1 or K2P3.1, is a member of the two-pore domain potassium (K2P) channel family that mediates background or "leak" potassium currents [1, 10]. These channels are constitutively active at resting membrane potentials and are essential for stabilizing the resting potential and adjusting cellular excitability in tissues such as the heart, lungs, and brain [5, 18]. K2P3.1 is uniquely sensitive to extracellular pH and hypoxia, functioning as a critical physiological sensor in the carotid body to regulate breathing [3, 7]. In the pulmonary circulation, K2P3.1 maintains the resting potential of smooth muscle cells, and its dysfunction—often due to KCNK3 gene mutations—is a primary driver of pulmonary arterial hypertension (PAH) [1, 9]. In the heart, K2P3.1 is predominantly expressed in the atria and contributes to action potential repolarization, making it a target for atrial-selective antiarrhythmic therapies [5, 8]. Pharmacological inhibition of the channel by drugs like carvedilol and amiodarone can prolong the action potential, while its activation by agents like treprostinil helps promote vasodilation [2, 6].

Other names

TASK-1TASK1TWIK-related acid-sensitive K+ channel 1TBAK1OAT1

K2P3.1 channels are background potassium channels that stabilize the resting membrane potential; inhibition leads to membrane depolarization and increased cellular excitability or prolongation of the action potential duration, whereas activation causes hyperpolarization and reduced excitability [5, 8, 9].