Inward rectifier potassium channel 2 (Kir2)

The Inward rectifier potassium channel 2 (Kir2) family, primarily comprising Kir2.1, Kir2.2, Kir2.3, and Kir2.4, plays a fundamental role in establishing and stabilizing the resting membrane potential in excitable tissues such as the heart, skeletal muscle, and brain (Source: UniProt P60507). These channels are characterized by their ability to conduct inward potassium currents more effectively than outward currents, a property known as inward rectification, which is mediated by the voltage-dependent block of the pore by intracellular magnesium and polyamines (Source: StatPearls, Potassium Channels). In the heart, the Kir2-mediated current (IK1) is crucial for the final phase of repolarization and the maintenance of a stable resting potential during diastole (Source: PubMed 21835018). Mutations in the genes encoding these channels, particularly KCNJ2, are linked to several channelopathies, including Andersen-Tawil syndrome (LQT7) and Short QT syndrome type 3, which manifest as cardiac arrhythmias and periodic paralysis (Source: NIH GeneReviews, KCNJ2-Related Disorders). Pharmacologically, Kir2 channels are targeted by various antiarrhythmic agents and are sensitive to blockade by compounds like chloroquine and flecainide (Source: PubMed 15618591, 22535919). Developing selective modulators for Kir2 channels remains a significant therapeutic interest for managing atrial and ventricular arrhythmias, though challenges persist regarding the potential for pro-arrhythmic side effects (Source: PubMed 28838934).

Other names

IRKKCNJStrong inward rectifier potassium channelIK1 channelKir2.1Kir2.2Kir2.3Kir2.4KCNJ2KCNJ12KCNJ4KCNJ14

Inhibition or modulation of the inward rectifier potassium current (IK1) to alter membrane excitability and action potential duration (Source: PubMed 21835018).