ArticlePflugers Archiv : European journal of physiology2005
Modulation of Na(v)1.5 by beta1-- and beta3-subunit co-expression in mammalian cells.
Article in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges.International journal of molecular sciences · 2024Review
- Cardiac sodium channel complexes and arrhythmia: structural and functional roles of the β1 and β3 subunits.The Journal of physiology · 2023Article
- The Antidepressant Paroxetine Reduces the Cardiac Sodium Current.International journal of molecular sciences · 2023Article
- Absolute Quantification of Nav1.5 Expression by Targeted Mass Spectrometry.International journal of molecular sciences · 2022Article
- Molecular Pathology of Sodium Channel Beta-Subunit Variants.Frontiers in pharmacology · 2021Article
- Cell-Adhesion Properties of β-Subunits in the Regulation of Cardiomyocyte Sodium Channels.Biomolecules · 2020Review
- Supramolecular clustering of the cardiac sodium channel Nav1.5 in HEK293F cells, with and without the auxiliary β3-subunit.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Life Cycle of the Cardiac Voltage-Gated Sodium Channel NaFrontiers in physiology · 2020Review
- AnFrontiers in cell and developmental biology · 2020Article
- Exploring the molecular basis of neuronal excitability in a vocal learner.BMC genomics · 2019Article
- Long Term Perinatal Deltamethrin Exposure Alters Electrophysiological Properties of Embryonic Ventricular Cardiomyocyte.Current medical science · 2019Article
- Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease.Neuropharmacology · 2018Review
- Voltage-Gated Sodium Channel β Subunits and Their Related Diseases.Handbook of experimental pharmacology · 2018Review
- Using fluorescence to understand β subunit-NaThe Journal of general physiology · 2017Article
- Pathogenic mechanism of recurrent mutations of SCN8A in epileptic encephalopathy.Annals of clinical and translational neurology · 2016Article
- Pharmacogenomics of cardiovascular complications in diabetes and obesity.Recent patents on biotechnology · 2014Review
- Cardiac sodium channelopathy associated with SCN5A mutations: electrophysiological, molecular and genetic aspects.The Journal of physiology · 2013Review
- Channelopathies from mutations in the cardiac sodium channel protein complex.Journal of molecular and cellular cardiology · 2013Review
- Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites.The Journal of biological chemistry · 2012Article
- A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Na(v)1.5 and K(v)4.3 channel currents.Heart rhythm · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac sodium channels (Na(v)1.5) comprise a pore-forming alpha-subunit and auxiliary beta-subunits that modulate channel function. In the heart, beta1 is expressed throughout the atria and ventricles, whilst beta3 is present only in the ventricles and Purkinje fibers. In view of this expression pattern, we determined the effects of beta3 and beta1 co-expression alone, and in combination, on Na(v)1.5 stably expressed in Chinese hamster ovary cells. The current/voltage relationship was shifted -5 mV with either beta1 or beta3 co-expression alone and -10 mV with co-expression of both beta1 and beta3. In addition, beta3 and beta1/beta3 co-expression accelerated macroscopic current decay. There were significant hyperpolarizing shifts in equilibrium gating relationships with co-expression of beta1 and beta3 alone and in combination. Co-expression of beta1/beta3 together resulted in a greater hyperpolarizing shift in channel availability, and an increase in the slopes of equilibrium gating relationships. Co-expression of beta3 and beta1/beta3, but not beta1, slowed recovery from inactivation at -90 mV. Development of inactivation at -70 and -50 mV was accelerated by beta-subunit co-expression alone and in combination. beta-Subunit co-expression also reduced the late Na current measured at 200 ms. In conclusion, beta-subunits modulate Na(v)1.5 gating with important differences between co-expression of beta1 and beta3 alone and beta1/beta3 together.
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