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Kir2.3 is an inwardly rectifying potassium channel encoded by the KCNJ4 gene, most prominent in cardiac and neuronal tissues. It allows potassium ions to enter cells more readily than exit, stabilizing negative resting membrane potential and contributing to repolarization during cardiac action potentials. Kir2.3 forms tetramers, often heteromerizing with other Kir2.x family members, and is regulated by proteins such as tax-interacting protein-1 (TIP-1). Dysfunction or aberrant regulation of Kir2.3 contributes to cardiovascular disorders (like arrhythmias) and possibly to neurological dysfunction and periodic paralysis. This channel is considered a therapeutic target—certain neurosteroids (pregnenolone sulfate) and small molecules (VU573) modulate Kir2.3 activity, with potential implications for drug development. Experimental compounds and classic blockers such as barium are used in research to study Kir2.3 pharmacology and electrophysiology.
Blockade of channel pore (e.g., barium blocks inward currents by obstructing the ion flow); Positive modulation of channel activity (pregnenolone sulfate increases Kir2.3 current); Inhibition of Kir2.3 by small molecules reduces potassium conductance and hyperpolarization
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