IKCa Assays

Background of IKCa channel

The intermediate conductance Ca²⁺-activated K channel, also known as IKCa or KCa 3.1, was considered an allosteric form of SKCa when it was first cloned in 1997 and was named SK4. In subsequent studies, people found an obvious difference in the conductance between SK4 and other SKCa channels, and it was further identified as IKCa. Like other K⁺ channels, the IKCa channel is involved in various processes in the body related to nerve and vascular function, and also be seen as a potential therapeutic drug target for Parkinson’s disease, ataxia, and hypertension.

Fig.1. Structure Prediction of the Human IKCa. (Uniprot ID O15554; obtained from Alphafold)

Distributions and Functions of IKCa

IKCa channel is meanly expressed in non-excitable cells such as vascular endothelial cells and secretory epithelial cells, studies have also shown the existence of a small amount of IKCa in excitatory cells such as nerve cells. IKCa channel plays a complex role in cell migration and death, neurotransmitter transmission, and maintenance of cell membrane potential.

Mechanisms of IKCa

IKCa channel senses Ca²⁺ signals and modulates membrane potential, cell volume, and Ca²⁺ or K⁺ concentration.

Channel	Gene	Mechanism	Activator	Blocker
IKCa	KCNN4	Unlike the BKCa or SKCa channels, the IKCa channel is voltage-independent. The opening of the IKCa channel is exclusively gated by the combination of Ca²⁺ and calmodulin with a moderate conductivity (30-80pS). IKCa channel can control cell membrane potential by directly regulating the Ca²⁺-dependent efflux of K⁺ or by modulating the driving force of Ca²⁺.	1-EBIO SKA 31	NS 6180 TRAM 34 TRM 39

Assay List of IKCa Channel

Creative Biolabs can provide a range of assays of the IKCa channel. You can choose the assay in the list or contact us for more information:

IKCa Channel

Assay No.	Assay Name	Host Cell	Assay Type	Datasheet
S01YF-0722-KX235	Magic™ Human KCNN4 In Vitro Electrophysiology Assay, CHO-K1	CHO-K1	Electrophysiology Assay

Published Data

Paper Title	Calmodulin antagonist W-7 enhances intermediate conductance Ca²⁺‑sensitive basolateral potassium channel (IKCa) activity in human colonic crypts
Journal	The Journal of Membrane Biology
Published	2021
Abstract	The intermediate conductance Ca²⁺-sensitive K⁺ channel (IKCa) dominates the K⁺ conductance of the basolateral membrane of human colonic crypts. These K⁺ channels are activated by increases in intracellular Ca²⁺ and cAMP and rapidly inhibited by aldosterone in a gene-independent manner. IKCa channels are highly sensitive to Ca²⁺ despite the lack of Ca²⁺ binding sites, which is achieved by the stimuli to channel subunits generated by conformational changes caused by intracellular Ca²⁺ binding calmodulin (CaM). Antagonists of CaM can reversibly bind the hydrophobic region of CaM to prevent the interaction between CaM and target proteins. However, correlation studies of the CaM antagonist W-7 with IKCa channel activity in previous experiments produced conflicting results. In response to this, the researchers experimentally assessed the effect of the CaM antagonist W-7 on Ca2+-mediated agonist-regulated basolateral IKCa channels in human colonic crypt cells.
Result	The researchers assessed the effect of W-7 on basolateral IKCa channels in human colonic crypt cells and performed patch clamp studies of IKCa channels in normally extracted intact crypt cells. IKCa channel activity studies showed that reducing bath Ca²⁺ from 1.2 mmol/L to 100 μmol/L in the absence of W-7 reversibly decreased IKCa channel activity, while in the presence of W-7 channel activity does not change at both bath Ca²⁺ concentrations. In a separate experiment, increasing bath calcium from 100mmolL/L to 1.2mmolL/L in the absence of W-7 reversibly increased the activity of μ channels, whereas, in the presence of W-7, channel activity was consistently high at both bath calcium concentrations. Experimental results showed that W-7 had a specific stimulatory effect on basolateral IKCa channel activity, although it was capable of inhibiting Ca²⁺/CaM-mediated IKCa channel-dependent Cl- secretion in human colonic epithelial cells. Fig.2. IKCa channel activity by patch clamp assay. (Kate, 2021)

Reference

Kate, A.B.; et al. Calmodulin antagonist W-7 enhances intermediate conductance Ca²⁺‑sensitive basolateral potassium channel (IKCa) activity in human colonic crypts. The Journal of Membrane Biology. 2021, 254: 423-428.

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