Hkv

hKv is an informal designation used in neuroscience to refer to human voltage-gated potassium channels, a broad superfamily of transmembrane proteins that conduct K+ ions in response to membrane depolarization. The hKv family includes multiple gene families, such as KCNA, KCNB, KCNC, KCND, KCNQ, and KCNT, giving rise to numerous channel subtypes named Kv1.x, Kv2.x, Kv3.x, Kv4.x, Kv7.x, and Kv9.x, among others. These channels are essential for shaping action potential repolarization and regulating neuronal and cardiac excitability.

Structurally, most hKv channels are tetramers of alpha subunits. Each subunit has six transmembrane segments (S1–S6); S4 acts as the voltage sensor, and the pore-forming region between S5 and S6 determines ion selectivity, commonly featuring the TVGYG motif. Auxiliary beta subunits can modulate gating, inactivation, and trafficking.

Diversity in biophysical properties underpins distinct physiological roles. Kv1 and Kv2 family members often provide delayed rectifier currents, Kv4 family members generate rapidly inactivating A-type currents, and Kv7 (KCNQ) channels underlie the noninactivating M-current. Together, hKv channels contribute to the resting membrane potential, spike timing, and neuronal firing patterns, and many are expressed in the heart where they influence repolarization.

Clinical relevance is broad: mutations in hKv genes are linked to epilepsy, ataxia, neuropathies, and cardiac arrhythmias such as Long QT syndrome (notably KCNQ1). Examples include KCNA1 mutations causing episodic ataxia type 1 and KCNQ2/3 mutations associated with neonatal seizures. Pharmacology often targets Kv channels with blockers like 4-aminopyridine or tetraethylammonium to study function or modulate excitability.

In research, hKv channels are studied using patch-clamp electrophysiology, mutagenesis, and structural methods such as cryo-EM, contributing to understanding of gating mechanisms and aiding drug discovery.