C-terminal interaction of KCNQ2 and KCNQ3 K+ channels
نویسندگان
چکیده
منابع مشابه
Regulation of the Voltage-gated K Channels KCNQ2/3 and KCNQ3/5 by Ubiquitination
form (Ekberg, J., Poronnik, P., Kumar, S., and Adams, D. J. (2005) J. Physiol. 567P, C91). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. 1 These authors contributed equally to this work. 2 To whom correspondence may...
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Channels from KCNQ2 and KCNQ3 genes have been suggested to underlie the neuronal M-type K(+) current. The M current is modulated by muscarinic agonists via G-proteins and an unidentified diffusible cytoplasmic messenger. Using whole-cell clamp, we studied tsA-201 cells in which cloned KCNQ2/KCNQ3 channels were coexpressed with M(1) muscarinic receptors. Heteromeric KCNQ2/KCNQ3 currents were mod...
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The voltage-gated KCNQ2/3 and KCNQ3/5 K(+) channels regulate neuronal excitability. We recently showed that KCNQ2/3 and KCNQ3/5 channels are regulated by the ubiquitin ligase Nedd4-2. Serum- and glucocorticoid-regulated kinase-1 (SGK-1) plays an important role in regulation of epithelial ion transport. SGK-1 phosphorylation of Nedd4-2 decreases the ability of Nedd4-2 to ubiquitinate the epithel...
متن کاملIdentification by mass spectrometry and functional characterization of two phosphorylation sites of KCNQ2/KCNQ3 channels.
Neuronal potassium channel subunits of the KCNQ (Kv7) family underlie M-current (I(M)), and may also underlie the slow potassium current at the node of Ranvier, I(Ks). I(M) and I(Ks) are outwardly rectifying currents that regulate excitability of neurons and myelinated axons, respectively. Studies of native I(M) and heterologously expressed Kv7 subunits suggest that, in vivo, KCNQ channels exis...
متن کاملPolarized axonal surface expression of neuronal KCNQ channels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminal domains.
The M channels, important regulators of neuronal excitability, are voltage-gated potassium channels composed of KCNQ2-5 subunits. Mutations in KCNQ2 and KCNQ3 cause benign familial neonatal convulsions (BFNC), dominantly inherited epilepsy and myokymia. Crucial for their functions in controlling neuronal excitability, the M channels must be placed at specific regions of the neuronal membrane. H...
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ژورنال
عنوان ژورنال: The Journal of Physiology
سال: 2003
ISSN: 0022-3751
DOI: 10.1113/jphysiol.2003.040980