AI Article Synopsis
- The study investigates how arachidonic acid metabolites activate specific potassium current (IK.ACh) in heart cells through G-protein channels.
- Co-expressing two types of G-protein-activated potassium channels (GIRKs) in frog oocytes confirmed that these channels can be activated by arachidonic acid metabolites, mimicking their behavior in heart cells.
- The findings suggest that these metabolites specifically target the GIRK1 subunit for activation, rather than through interactions with G-protein beta/gamma subunits.
Article Abstract
The molecular target of arachidonic-acid-derived metabolites, serving as second messengers that activate atrial acetylcholine-activated potassium current (IK.ACh) in addition to G-protein beta/gamma subunits (Gbeta/gamma), is unknown. Co-expression of two isoforms of G-protein-activated, inwardly rectifying potassium channels (GIRKs) in oocytes of Xenopus laevis revealed that these heterologous co-expressed GIRKs, which are responsible for the formation of IK.ACh in the atrium, are activated by arachidonic acid metabolites, like their counterparts in atrial cells. The expression of homooligomeric GIRK1(F137S) and GIRK4wt channels revealed that this activatory mechanism is specific to the GIRKI subunit. Sequestrating available Gbeta/gamma by overexpression of C-betaARK (a Gbeta/gamma binding protein) failed to abolish the activation of GIRK currents by arachidonic acid. From our experiments we conclude that the GIRKI subunit itself is the molecular target for regulation of GIRK channels by arachidonic acid metabolites.
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| http://dx.doi.org/10.1007/s004240000405 | DOI Listing |
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