Article
Kv7 channels can function without constitutive calmodulin tethering.
PloS one - 1 Jan 2011
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
Abstract excerpt
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...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
