Potassium inward rectifier channel subfamily J member 2 (Kir2.2)

The potassium inward rectifier channel subfamily J member 2 (Kir2.2, encoded by KCNJ2) is a tetrameric ion channel that allows K(+) ions to move more readily into cells than out, playing a critical role in maintaining the resting membrane potential of many cell types, especially cardiac and skeletal muscle cells[2][3][4][6]. Kir2.2 channels stabilize the membrane potential and are important for terminal repolarization during the cardiac action potential[4]. Channel opening is strongly dependent on binding of phosphatidylinositol 4,5-bisphosphate (PIP_2) at the interface between its transmembrane and cytoplasmic domains, which induces conformational changes to permit K(+) conduction[3][4][6]. Dysfunction or mutation of Kir2.2 (KCNJ2) is associated with inherited arrhythmia syndromes such as Andersen-Tawil syndrome and is also implicated in skeletal and smooth muscle excitability disorders[4]. Several drugs—including some antiarrhythmics—can interact with inward rectifier potassium channels and alter their function, which can pose risks of arrhythmia or be of therapeutic benefit in controlling abnormal heart rhythms[4]. The Kir2.2 channel is crucial for membrane stability, excitability, and the regulation of action potentials in excitable tissues[2][4].

Other names

KCNJ2Kir2.2Inward rectifier potassium channel 2IRK-2

Channel blockade (by antiarrhythmics, pharmacological inhibitors), Modulation of channel activity (via phospholipids such as PIP_2)