Potassium channel, inwardly rectifying subfamily J member 2 (KCNJ2)

Potassium channel, inwardly rectifying subfamily J member 2 (KCNJ2, also known as Kir2.1), encodes an inward-rectifier potassium channel integral to the stabilization of the resting membrane potential and the repolarization phase of action potentials in excitable cells, particularly in cardiac and skeletal muscle. It preferentially allows potassium ions to flow into rather than out of the cell, shaping cellular excitability. KCNJ2 is essential for maintaining rhythmic activity in the heart and normal muscle contraction. Mutations in KCNJ2 are linked to Andersen-Tawil syndrome (characterized by periodic paralysis, arrhythmias, and developmental defects), as well as other cardiac arrhythmias and short QT syndrome. Drugs targeting KCNJ2 act by blocking or modulating the channel, with known arrhythmogenic and muscle-related risks due to its key physiological roles[1][2][3][4][5][6][7][8].

Other names

Kir2.1IRK1

Blockade of potassium channel function (prevents potassium ion flow, prolongs cardiac action potential); Modulation of cardiac excitability (restoring or disrupting normal rhythm)