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Open Access item Kv7 Channels Can Function without Constitutive Calmodulin Tethering

Authors:Gómez Posada, Juan Camilo
Aivar, Paloma
Alberdi, Araitz
Alaimo, Alessandro
Etxeberría, Ainhoa
Fernández Orth, Juncal
Zamalloa, Teresa
Roura Ferrer, Meritxell
Villace, Patricia
Areso, Pilar
Casis, Oscar
Villarroel, Alvaro
Issue Date:28-Sep-2011
Publisher:Public Library of Science
Citation:PLoS ONE 6(9): e25508 (2011)
Abstract:M-channels are voltage-gated potassium channels composed of Kv7.2-7.5 subunits that serve as important regulators of neuronal excitability. Calmodulin binding is required for Kv7 channel function and mutations in Kv7.2 that disrupt calmodulin binding cause Benign Familial Neonatal Convulsions (BFNC), a dominantly inherited human epilepsy. On the basis that Kv7.2 mutants deficient in calmodulin binding are not functional, calmodulin has been defined as an auxiliary subunit of Kv7 channels. However, we have identified a presumably phosphomimetic mutation S511D that permits calmodulin-independent function. Thus, our data reveal that constitutive tethering of calmodulin is not required for Kv7 channel function.
Publisher version (URL):http://dx.doi.org/10.1371/journal.pone.0025508
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