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Proc Natl Acad Sci U S A
2012 Nov 06;10945:18577-82. doi: 10.1073/pnas.1209142109.
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Modulation of voltage-gated K+ channels by the sodium channel β1 subunit.
Nguyen HM, Miyazaki H, Hoshi N, Smith BJ, Nukina N, Goldin AL, Chandy KG.
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Voltage-gated sodium (Na(V)) and potassium (K(V)) channels are critical components of neuronal action potential generation and propagation. Here, we report that Na(V)β1 encoded by SCN1b, an integral subunit of Na(V) channels, coassembles with and modulates the biophysical properties of K(V)1 and K(V)7 channels, but not K(V)3 channels, in an isoform-specific manner. Distinct domains of Na(V)β1 are involved in modulation of the different K(V) channels. Studies with channel chimeras demonstrate that Na(V)β1-mediated changes in activation kinetics and voltage dependence of activation require interaction of Na(V)β1 with the channel's voltage-sensing domain, whereas changes in inactivation and deactivation require interaction with the channel's pore domain. A molecular model based on docking studies shows Na(V)β1 lying in the crevice between the voltage-sensing and pore domains of K(V) channels, making significant contacts with the S1 and S5 segments. Cross-modulation of Na(V) and K(V) channels by Na(V)β1 may promote diversity and flexibility in the overall control of cellular excitability and signaling.
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2009,
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2005,
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1997,
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2002,
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Pubmed Devaux,
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2005,
Pubmed Espinosa,
Ablation of Kv3.1 and Kv3.3 potassium channels disrupts thalamocortical oscillations in vitro and in vivo.
2008,
Pubmed Grissmer,
Pharmacological characterization of five cloned voltage-gated K+ channels, types Kv1.1, 1.2, 1.3, 1.5, and 3.1, stably expressed in mammalian cell lines.
1994,
Pubmed Gu,
Alternative splicing regulates kv3.1 polarized targeting to adjust maximal spiking frequency.
2012,
Pubmed Hoshi,
Voltage-dependent K+ currents and underlying single K+ channels in pheochromocytoma cells.
1988,
Pubmed Isom,
Primary structure and functional expression of the beta 1 subunit of the rat brain sodium channel.
1992,
Pubmed
,
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Isolation and sequence of a cDNA encoding the major structural protein of peripheral myelin.
1985,
Pubmed Lucas,
An epilepsy mutation in the beta1 subunit of the voltage-gated sodium channel results in reduced channel sensitivity to phenytoin.
2005,
Pubmed Luján,
Organisation of potassium channels on the neuronal surface.
2010,
Pubmed Marionneau,
The sodium channel accessory subunit Navβ1 regulates neuronal excitability through modulation of repolarizing voltage-gated K⁺ channels.
2012,
Pubmed McCormick,
The extracellular domain of the beta1 subunit is both necessary and sufficient for beta1-like modulation of sodium channel gating.
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,
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2002,
Pubmed
,
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BACE1 modulates filopodia-like protrusions induced by sodium channel beta4 subunit.
2007,
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Sodium channel beta4 subunit: down-regulation and possible involvement in neuritic degeneration in Huntington's disease transgenic mice.
2006,
Pubmed Patino,
A functional null mutation of SCN1B in a patient with Dravet syndrome.
2009,
Pubmed
,
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1999,
Pubmed Scheffer,
Temporal lobe epilepsy and GEFS+ phenotypes associated with SCN1B mutations.
2007,
Pubmed Song,
Acoustic environment determines phosphorylation state of the Kv3.1 potassium channel in auditory neurons.
2005,
Pubmed Vacher,
Localization and targeting of voltage-dependent ion channels in mammalian central neurons.
2008,
Pubmed Wallace,
Febrile seizures and generalized epilepsy associated with a mutation in the Na+-channel beta1 subunit gene SCN1B.
1998,
Pubmed
,
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