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The sodium channel beta-subunit SCN3b modulates the kinetics of SCN5a and is expressed heterogeneously in sheep heart.
Fahmi AI
,
Patel M
,
Stevens EB
,
Fowden AL
,
John JE
,
Lee K
,
Pinnock R
,
Morgan K
,
Jackson AP
,
Vandenberg JI
.
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1. Cardiac sodium channels are composed of a pore-forming alpha-subunit, SCN5a, and one or more auxiliary beta-subunits. The aim of this study was to investigate the role of the recently discovered member of the beta-subunit family, SCN3b, in the heart. 2. Northern blot and Western blot studies show that SCN3b is highly expressed in the ventricles and Purkinje fibres but not in atrial tissue. This is in contrast to the uniform expression of SCN1b throughout the heart. 3. Co-expression of SCN3b with the cardiac-specific alpha-subunit SCN5a in Xenopus oocytes resulted in a threefold increase in the level of functional sodium channel expression, similar to that observed when SCN1b was co-expressed with SCN5a. These results suggest that both SCN1b and SCN3b improve the efficiency with which the mature channel is targeted to the plasma membrane. 4. When measured in cell-attached oocyte macropatches, SCN3b caused a significant depolarising shift in the half-voltage of steady-state inactivation compared to SCN5a alone or SCN5a + SCN1b. The half-voltage of steady-state activation was not significantly different between SCN5a alone and SCN5a + SCN3b or SCN5a + SCN1b. 5. The rates of inactivation for SCN5a co-expressed with either subunit were not significantly different from that for SCN5a alone. However, recovery from inactivation at -90 mV was significantly faster for SCN5a + SCN1b compared to SCN5a + SCN3b, and both were significantly faster than SCN5a alone. 6. Thus, SCN1b and SCN3b have distinctive effects on the kinetics of activation and inactivation, which, in combination with the different patterns of expression of SCN3b and SCN1b, could have important consequences for the integrated electrical activity of the intact heart.
An,
Novel LQT-3 mutation affects Na+ channel activity through interactions between alpha- and beta1-subunits.
1998, Pubmed
An,
Novel LQT-3 mutation affects Na+ channel activity through interactions between alpha- and beta1-subunits.
1998,
Pubmed
Baroudi,
SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells.
2000,
Pubmed
,
Xenbase
Blount,
Assembly intermediates of the mouse muscle nicotinic acetylcholine receptor in stably transfected fibroblasts.
1990,
Pubmed
Brugada,
Sudden death in high-risk family members: Brugada syndrome.
2000,
Pubmed
Catterall,
From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels.
2000,
Pubmed
Chen,
Genetic basis and molecular mechanism for idiopathic ventricular fibrillation.
1998,
Pubmed
,
Xenbase
Dhar Malhotra,
Characterization of sodium channel alpha- and beta-subunits in rat and mouse cardiac myocytes.
2001,
Pubmed
Ellgaard,
Setting the standards: quality control in the secretory pathway.
1999,
Pubmed
Gellens,
Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel.
1992,
Pubmed
,
Xenbase
Isom,
Primary structure and functional expression of the beta 1 subunit of the rat brain sodium channel.
1992,
Pubmed
,
Xenbase
Isom,
Structure and function of the beta 2 subunit of brain sodium channels, a transmembrane glycoprotein with a CAM motif.
1995,
Pubmed
,
Xenbase
Makita,
Voltage-gated Na+ channel beta 1 subunit mRNA expressed in adult human skeletal muscle, heart, and brain is encoded by a single gene.
1994,
Pubmed
,
Xenbase
Marban,
Structure and function of voltage-gated sodium channels.
1998,
Pubmed
Morgan,
beta 3: an additional auxiliary subunit of the voltage-sensitive sodium channel that modulates channel gating with distinct kinetics.
2000,
Pubmed
,
Xenbase
Nuss,
Functional association of the beta 1 subunit with human cardiac (hH1) and rat skeletal muscle (mu 1) sodium channel alpha subunits expressed in Xenopus oocytes.
1995,
Pubmed
,
Xenbase
Patel,
Sodium channel isoform-specific effects of halothane: protein kinase C co-expression and slow inactivation gating.
2000,
Pubmed
,
Xenbase
Priori,
Long QT and Brugada syndromes: from genetics to clinical management.
2000,
Pubmed
Qu,
Modulation of cardiac Na+ channel expression in Xenopus oocytes by beta 1 subunits.
1995,
Pubmed
,
Xenbase
Sakmann,
Distribution of a persistent sodium current across the ventricular wall in guinea pigs.
2000,
Pubmed
Schott,
Cardiac conduction defects associate with mutations in SCN5A.
1999,
Pubmed
Stevens,
Tissue distribution and functional expression of the human voltage-gated sodium channel beta3 subunit.
2001,
Pubmed
,
Xenbase
Sutkowski,
Beta 1 subunits of sodium channels. Studies with subunit-specific antibodies.
1990,
Pubmed
Wallace,
Febrile seizures and generalized epilepsy associated with a mutation in the Na+-channel beta1 subunit gene SCN1B.
1998,
Pubmed
,
Xenbase
Wang,
SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome.
1995,
Pubmed
Watanabe,
Ventricular action potentials, ventricular extracellular potentials, and the ECG of guinea pig.
1985,
Pubmed
Wong,
Molecular and functional distributions of chloride conductances in rabbit ventricle.
1999,
Pubmed
