Functional and Molecular Aspects of Voltage‐Gated K<sup>+</sup> Channel β Subunits

Pongs, Olaf; Leicher, Thorsten; Berger, Michaela; Roeper, Jochen; Bähring, Robert; Wray, Dennis; Giese, Karl-Peter; Silva, Alcino J.; Storm, Johan F.

doi:10.1111/j.1749-6632.1999.tb11296.x

Cited by 187 publications

(139 citation statements)

References 33 publications

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“…Taking into account that Kv1.3AYA was able to reduce in a significant way the amplitude of the Kv1.4 currents when expressed in an heterologous system (Fig. 1), the lack of effect of Kv1.xDN on the O 2 -sensitive K ϩ current of rabbit CB chemoreceptor cells rules out a possible contribution of Kv1.4 channels to this current; moreover, we can also exclude the presence in the cells of heterotetrameric complexes of other members of the Kv1 subfamily that, in association with Kv␤ subunits, could give rise to rapidly inactivating currents, as described in other preparations (Pongs et al, 1999). However, the observed reduction in the magnitude of the noninactivating current in the Kv1.xDN-infected chemoreceptor cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells

et al. 2000

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Hypoxia initiates the neurosecretory response of the carotid body (CB) by inhibiting one or more potassium channels in the chemoreceptor cells. Oxygen-sensitive K ϩ channels were first described in rabbit CB chemoreceptor cells, in which a transient outward K ϩ current was reported to be reversibly inhibited by hypoxia. Although progress has been made to characterize this current with electrophysiological and pharmacological tools, no attempts have been made to identify which Kv channel proteins are expressed in rabbit CB chemoreceptor cells and to determine their contribution to the native O 2 -sensitive K ϩ current. To probe the molecular identity of this current, we have used dominantnegative constructs to block the expression of functional Kv channels of the Shaker (Kv1.xDN) or the Shal (Kv4.xDN) subfamilies, because members of these two subfamilies contribute to the transient outward K ϩ currents in other preparations. Delivery of the constructs into chemoreceptor cells has been achieved with adenoviruses that enabled ecdysone-inducible expression of the dominant-negative constructs and reporter genes in polycistronic vectors. In voltage-clamp experiments, we found that, whereas adenoviral infections of chemoreceptor cells with Kv1.xDN did not modify the O 2 -sensitive K ϩ current, infections with Kv4.xDN suppressed the transient outward current in a time-dependent manner, significantly depolarized the cells, and abolished the depolarization induced by hypoxia. Our work demonstrate that genes of the Shal K ϩ channels underlie the transient outward, O 2 -sensitive, K ϩ current of rabbit CB chemoreceptor cells and that this current contributes to the cell depolarization in response to low pO 2 .

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Section: Discussionmentioning

confidence: 99%

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells

et al. 2000

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“…Recent genetic studies have established a clear inverse relationship between QT interval and expression and function of potassium channels. Gene defects resulting in loss of function of voltage‐gated potassium channels, for example, are associated with long QT syndromes: LQT1 (KCNQ1) and LQT2 (KCNH2), encoding α‐subunits of the potassium channels I Ks and I Kr ; LQT5 (KCNE1) and LQT6 (KCNE2), encoding β‐subunits of the potassium channels I Ks and I Kr ; and LQT7 (KCNJ2), encoding the inward rectifier potassium channel Kir2.1 12, 13, 14, 15, 16, 17…”

Section: Discussionmentioning

confidence: 99%

Obstructive Sleep Apnea and Circulating Potassium Channel Levels

Zhou

Prasad

et al. 2016

JAHA

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BackgroundCardiac arrhythmias and sudden cardiac death are more frequent in patients with obstructive sleep apnea (OSA). OSA is associated with QT prolongation, and QT prolongation is an independent risk factor for sudden cardiac death. Because QT prolongation can be mediated by potassium channel loss of function, we tested whether OSA or continuous positive airway pressure therapy altered mRNA expression of circulating white blood cell potassium channels.Methods and ResultsIn total, 28 patients with OSA newly diagnosed by polysomnogram and 6 participants without OSA were enrolled. Potassium channel levels in white blood cells at baseline and at a 4‐week follow‐up visit were compared. There was a significant inverse correlation between the severity of the OSA stratified by apnea–hypopnea index and mRNA expression of the main potassium channels assessed: KCNQ1 (r=−0.486, P=0.007), KCNH2 (r=−0.437, P=0.016), KCNE1 (r=−0.567, P=0.001), KCNJ2 (r=−0.442, P=0.015), and KCNA5 (r=−0.468, P=0.009). In addition, KCNQ1, KCNH2, and KCNE1 inversely correlated with the oxygen desaturation index 4. After 4 weeks of continuous positive airway pressure therapy, circulating KCNQ1 and KCNJ2 were increased 1.4±0.4‐fold (P=0.040) and 2.1±1.4‐fold (P=0.046) in the moderate OSA group. Compared with patients with mild or moderate OSA, patients with severe OSA had a persistently higher apnea–hypopnea index (mild 2.0±1.8, moderate 1.0±0.9, severe 5.8±5.6; P=0.015), perhaps explaining why the potassium channel changes were not seen in the severe OSA group.ConclusionsThe mRNA expression of most potassium channels inversely correlates with the severity of OSA and hypoxemia. Continuous positive airway pressure therapy improves circulating KCNQ1 and KCNJ2 in patients with moderate OSA.

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“…Two members of the voltage-sensitive K ϩ channel family (Pongs et al, 1999) were detected in different patterns at st. 2 ϩ : Kv3.1 is strongly expressed in the primitive streak (Fig. 1K), and Kv6.2 is present in the base of the streak (Fig.…”

Section: Expression Of Ion Channels and Pumps In Early Embryosmentioning

confidence: 99%

Early embryonic expression of ion channels and pumps in chick and Xenopus development

Rutenberg

Cheng²,

Levin³

2002

Developmental Dynamics

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An extensive body of literature implicates endogenous ion currents and standing voltage potential differences in the control of events during embryonic morphogenesis. Although the expression of ion channel and pump genes, which are responsible for ion flux, has been investigated in detail in nervous tissues, little data are available on the distribution and function of specific channels and pumps in early embryogenesis. To provide a necessary basis for the molecular understanding of the role of ion flux in development, we surveyed the expression of ion channel and pump mRNAs, as well as other genes that help to regulate membrane potential. Analysis in two species, chick and Xenopus, shows that several ion channel and pump mRNAs are present in specific and dynamic expression patterns in early embryos, well before the appearance of neurons. Examination of the distribution of maternal mRNAs reveals complex spatiotemporal subcellular localization patterns of transcripts in early blastomeres in Xenopus. Taken together, these data are consistent with an important role for ion flux in early embryonic morphogenesis; this survey characterizes candidate genes and provides information on likely embryonic contexts for their function, setting the stage for functional studies of the morphogenetic roles of ion transport.

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Functional and Molecular Aspects of Voltage‐Gated K⁺ Channel β Subunits

Cited by 187 publications

References 33 publications

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells

Obstructive Sleep Apnea and Circulating Potassium Channel Levels

Early embryonic expression of ion channels and pumps in chick and Xenopus development

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Functional and Molecular Aspects of Voltage‐Gated K+ Channel β Subunits

Cited by 187 publications

References 33 publications

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O2-Sensitive K+Current in Chemoreceptor Cells

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O2-Sensitive K+Current in Chemoreceptor Cells

Obstructive Sleep Apnea and Circulating Potassium Channel Levels

Early embryonic expression of ion channels and pumps in chick and Xenopus development

Contact Info

Product

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Functional and Molecular Aspects of Voltage‐Gated K⁺ Channel β Subunits

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells

Viral Gene Transfer of Dominant-Negative Kv4 Construct Suppresses an O₂-Sensitive K⁺Current in Chemoreceptor Cells