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Title

An ether -a-go-go K+ current, Ih-eag, contributes to the hyperpolarization of human fusion-competent myoblasts

Authors
Bijlenga, P.
Occhiodoro, T.
Liu, J. H.
Published in The Journal of Physiology. 1998, vol. 512, no. 2, p. 317-323
Abstract 1. Two early signs of human myoblast commitment to fusion are membrane potential hyperpolarization and concomitant expression of a non-inactivating delayed rectifier K+ current, IK(NI). This current closely resembles the outward K+ current elicited by rat ether-a-go-go (r-eag) channels in its range of potential for activation and unitary conductance. 2. It is shown that activation kinetics of IK(NI), like those of r-eag, depend on holding potential and on [Mg2+]o, and that IK(NI), like r-eag, is reversibly inhibited by a rise in [Ca2+]i. 3. Forced expression of an isolated human ether-a-go-go K+ channel (h-eag) cDNA in undifferentiated myoblasts generates single-channel and whole-cell currents with remarkable similarity to IK(NI). 4. h-eag current (Ih-eag) is reversibly inhibited by a rise in [Ca2+]i, and the activation kinetics depend on holding potential and [Mg2+]o. 5. Forced expression of h-eag hyperpolarizes undifferentiated myoblasts from -9 to -50 mV, the threshold for the activation of both Ih-eag and IK(NI). Similarly, the higher the density of IK(NI), the more hyperpolarized the resting potential of fusion-competent myoblasts. 6. It is concluded that h-eag constitutes the channel underlying IK(NI) and that it contributes to the hyperpolarization of fusion-competent myoblasts. To our knowledge, this is the first demonstration of a physiological role for a mammalian eag K+ channel.
Keywords AdolescentAlgorithmsAnimalsCalcium/metabolismCell Differentiation/physiologyCell Fusion/physiologyCell Polarity/ physiologyCells, CulturedChildChild, PreschoolElectric StimulationElectrophysiologyEther-A-Go-Go Potassium ChannelsHumansInfantMembrane Potentials/physiologyMuscle DevelopmentMuscle, Skeletal/cytology/growth & development/ metabolismPatch-Clamp TechniquesPotassium Channels/ metabolismRats
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Other version: http://jp.physoc.org/content/512/2/317.abstract
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PMID: 9763622
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