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Potassium voltage-gated channel subfamily G member 2 (KCNG2) is an electrically silent regulatory subunit of voltage-gated potassium (Kv) channels belonging to subfamily G. Unlike pore-forming α-subunits, KCNG2 does not form functional channels alone but modulates the properties of channel complexes when coassembled, particularly with KCNB1/Kv2.1. It contributes to the delayed rectifier potassium current, especially in the heart, affecting cardiac action potential repolarization. KCNG2 is implicated in cardiovascular physiology, neuropsychiatric disease, and cellular responses to stress, and variants have been linked to diseases such as sick sinus syndrome and opioid dependence. It acts by fine-tuning the activity of potassium channels, and drugs such as propafenone modulate its function when incorporated into channel complexes[3][2][4][5][6].
Channel modulation by forming heterotetramers with other voltage-gated potassium channel α-subunits (notably KCNB1/Kv2.1), altering the kinetics and properties of the channel complex. Inhibition of overall potassium current amplitude by dominant-negative modulation
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