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Title

Kv7 Channels Can Function without Constitutive Calmodulin Tethering

AuthorsGómez 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 Date28-Sep-2011
PublisherPublic Library of Science
CitationPLoS ONE 6(9): e25508 (2011)
AbstractM-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
URIhttp://hdl.handle.net/10261/44319
DOI10.1371/journal.pone.0025508
ISSN1932-6203
Appears in Collections:(UBF) Artículos
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