Kv3.4 is a member of the voltage-gated K+ channel superfamily. Together with the related proteins Kv3.1, Kv3.2 and Kv3.3they constitute the Shaw type subfamily family.1
As with all Kv channels, Kv3.4 possesses the signature structure of the voltage-dependent K+ channels: six membrane-spanning domains with intracellular N and C termini. The functional Kv channel is a tetramer that can either be a homomer or a heteromer of Kv3 subunits.2
Kv3 subfamily members inactivate very rapidly and therefore are thought to play a role in the repolarization of action potentials and to facilitate repetitive high frequency firing.2
Kv3.4 expression is wide and the channel can be found in brain, skeletal muscle, prostate and pancreas among others.
Kv3.4 subunits have been implicated recently in the response mechanism to chronic hypoxia and the etiology of Alzheimer's and Parkinson's diseases. In addition, Kv3.4 was found to associate with the auxiliary subunit KCNE3 (MirP2) in skeletal muscle. A mutation in KCNE3 (R83H) has been associated with an inherited form of periodic paralysis (Thyrotoxic hypokalemic periodic paralysis) that is caused by the altered physiological function of the Kv3.4 channel.3
Toxins from sea anemone, BDS-I (#B-400), (47nM) and BDS-II (#B-450), (56nM), are potent blockers of KV3.4 channels.4
