Abstract
We have studied the properties of r-eag voltage-activated potassium channels in a stably transfected human embryonic kidney cell line. It was found that r-eag channels are rapidly and reversibly inhibited by a rise in intracellular calcium from 30 to 300 nM. The inhibition does not appear to depend on the activity of calcium-dependent kinases and phosphatases. The effect of calcium on r-eag channel activity was studied in inside-out membrane patches. Calcium inhibited r-eag channel activity with a mean IC50 of 67 nM. Activation of muscarinic receptors, generating calcium oscillations in the transfected cells, induced a synchronous inhibition of r-eag mediated outward currents. This shows that calcium can mediate r-eag current inhibition following muscarinic receptor activation. The data indicate that r-eag channels are calcium-inhibitable voltage-activated potassium channels.
MeSH Terms
Animals
Calcium/metabolism
Cell Line
Electrophysiology
Ether-A-Go-Go Potassium Channels
Humans
Ionomycin/pharmacology
Kidney/cytology,metabolism
Potassium Channels/metabolism
Rats
Receptors, Muscarinic/metabolism
Spectrometry, Fluorescence
Transfection
Chemicals
Ether-A-Go-Go Potassium Channels
Potassium Channels
Receptors, Muscarinic
Ionomycin
Calcium
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Stansfeld C E
Zentrum für Moleculare Neurobiologie, Universität Hamburg, Germany.
Röper J
Ludwig J
Weseloh R M
Marsh S J
Brown D A
Pongs O
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