SKCa Assays

Background of SKCa Channel

SKCa channel is a kind of K⁺ channel that can only be activated by a low level of intracellular Ca²⁺ concentration with no sensitivity to changes in membrane voltage. SKCa channel plays a critical role in many physiological and pathological processes, such as cardio and vascular capacity regulation, prevention, and treatment of neurological diseases.

Fig.1. Structure Prediction of the Human SK1. (Uniprot ID Q92952; obtained from Alphafold)

Distributions and Functions of SKCa

SKCa channel is widely distributed in the central nervous system, but can also be detected in various cell types in the peripheral nervous system, especially in the T lymphocytes, the glandular cells, or the skeletal muscle cells. In nerve cells or other excitable cells, the SKCa channel adjusts K⁺ concentration thus inducing repolarization or hyperpolarization to inhibit the excitability of voltage-gated Ca²⁺ channels, thereby reducing intracellular Ca²⁺ concentration, while in non-excitable cells, the SKCa channel increases the driving force of Ca²⁺ through voltage-gated Ca²⁺ channels, and then increase the concentration of intracellular Ca²⁺.

Submembers and Mechanisms of SKCa

There are three sets of genes encoding three different SK proteins in mammals, all of which are similar in function and structure.

Channel	Gene	Mechanism	Activator	Blocker
SKCa1	KCNN1	SCKa channel shows little sensitivity to cell membrane voltage but can be activated when free calcium concentration reaches a certain level. SKCa can mediate the hyperpolarization of cell membranes with a smaller conductance (10pS).	EBIO GW 542573X SKA 31	Apamin UCL 1684
SKCa2	KCNN2		CyPPA 1-EBIO SKA 31	Apamin UCL 1684 Lei-Dab 7
SKCa3	KCNN3		CyPPA 1-EBIO SKA 31	Apamin UCL 1684

Assay List of SKCa Channel

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

SKCa Channels

Assay No.	Assay Name	Host Cell	Assay Type
S01YF-0722-KX232	Magic™ Human KCNN1 In Vitro Electrophysiology Assay		Electrophysiology Assay
S01YF-0722-KX233	Magic™ Human KCNN2 In Vitro Electrophysiology Assay, HEK293	HEK293	Electrophysiology Assay
S01YF-0722-KX234	Magic™ Human KCNN3 In Vitro Electrophysiology Assay		Electrophysiology Assay

Published Data

Paper Title	Reduced activity of SKCa and Na-K ATPase underlies the accelerated impairment of EDH-type relaxations in mesenteric arteries of aging spontaneously hypertensive rats
Journal	Pharmacology Research & Perspectives
Published	2015
Abstract	Endothelial cells regulate inflammation and angiogenesis in vivo and modulate vascular tone through vasodilator and vasoconstrictor signals. Healthy endothelial cells maintain a balance between the release of contractile factors and relaxing factors in response to various endogenous or exogenous stimuli. Studies have shown that vasodilation is achieved by nitric oxide produced by endothelial NO synthase (eNOS) and endothelium-dependent hyperpolarization (EDH). Long-term exposure to hypertensive states accelerates endothelial cell senescence, leading to a deterioration of endothelial function and changes in derived vasoactive substances. Previous studies have shown that the silent information regulator (SIRT1) activates eNOS and induces NO production, which leads to a relaxation of blood vessels. In addition, the endothelial AMPK gene has also been confirmed to play a role in the EDH signaling pathway. Based on the facts, this experiment focused on endothelial dysfunction and the signaling pathways leading to vascular relaxation under natural aging and hypertension, and confirmed the role of SKCa channels in the process of vascular relaxation.
Result	The experiment selected aged rats and hypertensive rats as animal models to verify vascular injury under different conditions. The data suggest that EDH-mediated vascular relaxation in rat mesenteric arteries undergoes hypertension-mediated or age-dependent impairment and is exacerbated in the coexistence of both. Further verification of the phenomenons found that both exhibited low functional activity of SKCa channels, which may be responsible for impaired endothelial function. Furthermore, EDH relaxation in young hypertensive animals is largely dependent on the activation of SIRT1 and AMPK, which identifies a role for SIRT1 and AMPK in the progressive impairment of endothelium-dependent relaxation. Altogether, this experiment better elucidates the underlying events of endothelial dysfunction that progresses with aging and its acceleration due to hypertension, and will help in the design of pharmacological interventions to reduce/prevent vascular complications in the elderly. Fig.2. Mechanisms of impaired endothelium-dependent hyperpolarization (EDH)-type relaxation in aging or hypertensive rats based on experimental results. (Kong, 2015)

Reference

Kong, B.W.C.; et al. Reduced activity of SKCa and Na-K ATPase underlies the accelerated impairment of EDH-type relaxations in mesenteric arteries of aging spontaneously hypertensive rats. Pharmacology Research & Perspectives. 2015, 3(3): e00150.

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