Kv7 Channels Can Function without Constitutive Calmodulin Tethering
Data(s) |
09/01/2013
09/01/2013
28/09/2011
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Resumo |
9 p. 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. |
Identificador |
PLoS ONE 6(9) : (2011) // e25508 1932-6203 http://hdl.handle.net/10810/9207 10.1371/journal.pone.0025508 |
Idioma(s) |
eng |
Publicador |
Public Library of Science |
Relação |
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0025508 |
Direitos |
© 2011 Gomez-Posada et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. info:eu-repo/semantics/openAccess |
Palavras-Chave | #Ca2+-activated K+ channels #go potassium channels #surface expression #cell-surface #human ether #trafficking #binding #inhibition #subunit |
Tipo |
info:eu-repo/semantics/article |