Genomic analyses of sodium channel α-subunit genes from strains of melon thrips, Thrips palmi, with different sensitivities to cypermethrin

Molecular medicine requires the precise definition of drug targets, and tools are now in place to provide genome-wide information on the expression and alternative splicing patterns of any known gene. DNA microarrays were used to monitor transcript levels of the nine well-characterized α-subunit sodium channel genes across a broad range of tissues from cynomolgus monkey, a non-human primate model. Alternative splicing of human transcripts for a subset of the genes that are expressed in dorsal root ganglia, SCN8A (Nav1.6), SCN9A (Nav1.7), and SCN11A (Nav1.9) was characterized in detail. Genomic sequence analysis among gene family paralogs and between cross-species orthologs suggested specific alternative splicing events within transcripts of these genes, all of which were experimentally confirmed in human tissues. Quantitative PCR revealed that certain alternative splice events are uniquely expressed in dorsal root ganglia. In addition to characterization of human transcripts, alternatively spliced sodium channel transcripts were monitored in a rat model for neuropathic pain. Consistent down-regulation of all transcripts was observed, as well as significant changes in the splicing patterns of SCN8A and SCN9A.

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Differential Regulation of the Epithelial Sodium Channel (ENaC) in Rat Kidney, Lung and Distal Colon in Response to Aldosterone.

Hypertension ◽

10.1161/hyp.36.suppl_1.724 ◽

2000 ◽

Vol 36 (suppl_1) ◽

pp. 724-724

Author(s):

Shyama M E Masilamani ◽

Gheun-Ho Kim ◽

Mark A Knepper

Keyword(s):

Sodium Channel ◽

Epithelial Sodium Channel ◽

Distal Colon ◽

Β Subunit ◽

Dietary Salt ◽

Α Subunit ◽

Salt Restriction ◽

Γ Subunit ◽

Dietary Salt Restriction ◽

Epithelial Sodium Channel Enac

P170 The mineralocorticoid hormone, aldosterone increases renal tubule Na absorption via increases in the protein abundances of the α-subunit of the epithelial sodium channel (ENaC) and the 70 kDa form of the γ- subunit of ENaC (JCI 104:R19-R23). This study assesses the affect of dietary salt restriction on the regulation of the epithelial sodium channel (ENaC) in the lung and distal colon, in addition to kidney, using semiquantitative immunoblotting. Rats were placed initially on either a control Na intake (0.02 meq/day), or a low Na intake (0.2 meq/day) for 10 days. The low salt treated rats demonstrated an increase in plasma aldosterone levels at day 10 (control = 0.78 + 0.32 nM; Na restricted = 3.50 + 1.30 nM). In kidney homogenates, there were marked increases in the band density of the α-subunit of ENaC (286 % of control) and the 70 kDa form of γ-subunit of ENaC (262 % of control), but no increase in the abundance of the β-subunit of ENaC. In lung homogenates, there was no significant change in the band densities of the α, β, or γ subunits of ENaC. In distal colon, there was an increase in the band density of the β-subunit of ENaC (311 % of control) and an increase in both the 85 kDa (2355% of control) and 70 kDa (843 % of control) form of the γ subunit of ENaC in response to dietary Na restriction. However, there was no significant difference in the band density of the α-subunit of ENaC. These findings demonstrate tissue specific regulation of the three subunits of ENaC in response to dietary salt restriction.

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Insulin-induced phosphorylation of ENaC correlates with increased sodium channel function in A6 cells

AJP Cell Physiology ◽

10.1152/ajpcell.00343.2004 ◽

2005 ◽

Vol 288 (1) ◽

pp. C141-C147 ◽

Cited By ~ 33

Author(s):

Yu-Hua Zhang ◽

Diego Alvarez de la Rosa ◽

Cecilia M. Canessa ◽

John P. Hayslett

Keyword(s):

Sodium Channel ◽

Sodium Transport ◽

Polyclonal Antibodies ◽

Hormonal Stimulation ◽

Α Subunit ◽

A6 Cells ◽

Kinase C ◽

Sds Page ◽

Protein Kinase C Inhibitor ◽

Synergistic Increase

The purpose of this study was to determine whether there is a correlation between phosphorylation and activity of the epithelial sodium channel (ENaC). The three subunits that form the channel were immunoprecipitated from A6 cells by using specific polyclonal antibodies after labeling cells with 35S or 32P. When immune complexes were resolved on SDS-PAGE, the α-subunit migrated at 85 and 65 kDa, the β-subunit at 115 and 100 kDa, and the γ-subunit at 90 kDa. In the resting state all three subunits were phosphorylated. The α-subunit was phosphorylated only in the 65-kDa band, suggesting that the posttranslational modification that gives rise to the rapidly migrating form of α is a requirement for phosphorylation. Stimulation with 100 nM insulin for 30 min increased phosphorylation of α-, β-, and γ-subunits approximately twofold. Exposure to 1 μM aldosterone for 16 h increased protein abundance and phosphorylation proportionately in the three subunits. When insulin was applied to cells pretreated with aldosterone, phosphorylation was also increased approximately twofold, but the total amount of phosphorylated substrate was larger than in control conditions because of the action of aldosterone. This result might explain the synergistic increase in sodium transport under the same conditions. The protein kinase C inhibitor chelerythrine abolished insulin effects and decreased sodium transport and subunit phosphorylation. Together, our findings suggest that ENaC activity is controlled by subunit phosphorylation in cells that endogenously express the channel and the machinery for hormonal stimulation of sodium transport.

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Control of melon thrips, Thrips palmi Karny on greenhouse eggplant by releasing of Amblyseius swirskii Athias-Henriot

Annual Report of The Kansai Plant Protection Society ◽

10.4165/kapps.52.21 ◽

2010 ◽

Vol 52 ◽

pp. 21-25 ◽

Cited By ~ 1

Author(s):

Manabu Shibao ◽

Tetsuya Adachi ◽

Kiyotsugu Okada ◽

Hyoya Hayashi ◽

Yutaka Kubota ◽

...

Keyword(s):

Amblyseius Swirskii ◽

Thrips Palmi ◽

Melon Thrips

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Cardiac sodium channel, its mutations and their spectrum of arrhythmia phenotypes

Journal of Human Growth and Development ◽

10.7322/jhgd.122759 ◽

2016 ◽

Vol 26 (3) ◽

pp. 281 ◽

Cited By ~ 1

Author(s):

Andrés Ricardo Pérez-Riera ◽

Rodrigo Daminello Raimundo ◽

Rodrigo Akira Watanabe ◽

José Luiz Figueiredo ◽

Luiz Carlos de Abreu

Keyword(s):

Sodium Channel ◽

Cardiac Muscle ◽

Heart Function ◽

Heart Diseases ◽

Cardiac Conduction ◽

Activation Process ◽

Α Subunit ◽

Cardiac Sodium Channel ◽

Wide Range ◽

Scn5a Gene

The mechanisms of cellular excitability and propagation of electrical signals in the cardiac muscle are very important functionally and pathologically. The heart is constituted by three types of muscle: atrial, ventricular, and specialized excitatory and conducting fi bers. From a physiological and pathophysiological point of view, the conformational states of the sodium channel during heart function constitute a signifi cant aspect for the diagnosis and treatment of heart diseases. Functional states of the sodium channel (closed, open, and inactivated) and their structure help to understand the cardiac regulation processes. There are areas in the cardiac muscle with anatomical and functional differentiation that present automatism, thus subjecting the rest of the fi bers to their own rhythm. The rate of these (pacemaker) areas could be altered by modifi cations in ions, temperature and especially, the autonomic system. Excitability is a property of the myocardium to react when stimulated. Another electrical property is conductivity, which is characterized by a conduction and activation process, where the action potential, by the all-or-nothing law, travels throughout the heart. Heart relaxation also stands out as an active process, dependent on the energetic output and on specificion and enzymatic actions, with the role of sodium channel being outstanding in the functional process. In the gene mutation aspects that encode the rapid sodium channel (SCN5A gene), this channel is responsible for several phenotypes, such as Brugada syndrome, idiopathic ventricular fibrillation, dilated cardiomyopathy, early repolarization syndrome, familial atrial fibrillation, variant 3 of long QT syndrome, multifocal ectopic ventricular contractions originating in Purkinje arborizations, progressive cardiac conduction defect (Lenègre disease), sudden infant death syndrome, sick sinus syndrome, sudden unexplained nocturnal death syndrome, among other sodium channel alterations with clinical overlapping. Finally, it seems appropriate to consider the “sodium channel syndrome” (mutations in the gene of the α subunit of the sodium channel, SCN5A gene) as a single clinical entity that may manifest in a wide range of phenotypes, to thus have a better insight on these cardiac syndromes and potential outcomes for their clinical treatment.

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