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• W2187718641 abstract "MutationsinKCNQ2andKCNQ3voltage-gatedpotassiumchannelslead to neonatal epilepsy as a consequence of their key role inregulating neuronal excitability. Previous studies in the brain havefocusedprimarilyontheseKCNQfamilymembers,whichcontributeto M-currents and afterhyperpolarization conductances in multiplebrain areas. In contrast, the function of KCNQ5 (Kv7.5), which alsodisplays widespread expression in the brain, is entirely unknown.Here, we developed mice that carry a dominant negative mutationintheKCNQ5poretoprobewhetherithasasimilarfunctionasotherKCNQ channels. This mutation renders KCNQ5" @default.
• W2187718641 created "2016-06-24" @default.
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• W2187718641 date "2010-01-01" @default.
• W2187718641 modified "2023-09-27" @default.
• W2187718641 title "The KCNQ5 potassium channel mediates a component of the afterhyperpolarization current in mouse" @default.
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