Target intelligence / Profile preview

Squid axon voltage-gated potassium channel (SqKv1.1)

Target
SqKv1.1
Molecular classification
Ion channel, Voltage-gated potassium channel, Kv1 family
01

Overview

The squid axon voltage-gated potassium channel is a foundational model in neurobiology, famously characterized by Alan Hodgkin and Andrew Huxley in their Nobel Prize-winning work on the action potential [1]. Located in the giant axon of squids such as Loligo pealeii, this channel is a member of the Kv1 (Shaker-related) family and functions as a 'delayed rectifier' (IK) [2]. Its primary biological role is to mediate the efflux of potassium ions following membrane depolarization, which is essential for the rapid repolarization of the action potential and the maintenance of the resting membrane potential [1]. Although it is not a human therapeutic target, its study has provided the fundamental biophysical principles for understanding human voltage-gated potassium channels, such as KCNA1 (Kv1.1), which are critical in various neurological and cardiovascular diseases [2]. The channel is a classic pharmacological target for blockers such as tetraethylammonium (TEA) and 4-aminopyridine (4-AP), which inhibit the channel by occluding the ion-conducting pore [3]. These interactions have been instrumental in mapping the pore structure and gating mechanisms of ion channels across species [2]. [1] Hodgkin and Huxley, Journal of Physiology, 1952; [2] Rosenthal and Gilly, Proceedings of the National Academy of Sciences, 2003; [3] UniProtKB, Q26657.

Other names
Delayed rectifier potassium channelIKSquid giant axon potassium channelSqKv1Potassium voltage-gated channel protein 1Shaker-related potassium channel
02

Mechanism of action

Pore blockade of the potassium channel, leading to inhibition of potassium efflux and prolongation of the action potential duration.

03

Biological functions

Action potential repolarizationPotassium ion transportRegulation of membrane potentialRegulation of neuronal excitability
04

Disease associations

None
05

Safety considerations

NeurotoxicityLack of selectivity for human homologs
06

Interacting drugs

Tetraethylammonium

2 more in the full profile.

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