O<sub>2</sub>‐sensitive K<sup>+</sup> channels: role of the Kv1.2 α‐subunit in mediating the hypoxic response

Conforti, Laura; Bódi, Ilona; Nisbet, John W.; Millhorn, David E.

doi:10.1111/j.1469-7793.2000.00783.x

Cited by 93 publications

(78 citation statements)

References 45 publications

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“…Charybdotoxin, a blocker of Kv1.2, inhibits the oxygen-sensitive K z current in PC12 cells [34]. Moreover, intracellular administration of an anti-Kv1.2 antibody completely abolishes this current, while an anti-Kv2.1 antibody has no effect [34]. Finally, hypoxia inhibits Kv1.2 when expressed in Xenopus oocytes, although it fails to affect Kv2.1 [34].…”

Section: Molecular Diversity Of Potassium Channels B Subunitsmentioning

confidence: 99%

“…Moreover, cells maintained in chronic hypoxia become more responsive to a subsequent acute hypoxia when compared to cells maintained in normoxia [33]. Charybdotoxin, a blocker of Kv1.2, inhibits the oxygen-sensitive K z current in PC12 cells [34]. Moreover, intracellular administration of an anti-Kv1.2 antibody completely abolishes this current, while an anti-Kv2.1 antibody has no effect [34].…”

Section: Molecular Diversity Of Potassium Channels B Subunitsmentioning

confidence: 99%

“…Both carotid body type I cells and pheochromocytoma PC12 cells originate from neural crest and synthesize dopamine as their major neurotransmitter response in low partial oxygen pressure (PO 2 ) conditions [33,34] [33,34] ( fig. 1).…”

Section: Molecular Diversity Of Potassium Channels B Subunitsmentioning

confidence: 99%

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Molecular physiology of oxygen-sensitive potassium channels

2001

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Physiological adaptation to acute hypoxia involves oxygen-sensing by a variety of specialized cells including carotid body type I cells, pulmonary neuroepithelial body cells, pulmonary artery myocytes and foetal adrenomedullary chromaffin cells.Hypoxia induces depolarization by closing a specific set of potassium channels and triggers cellular responses. Molecular biology strategies have recently allowed the identification of the K z channel subunits expressed in these specialized cells. Several voltage-gated K z channel subunits comprising six transmembrane segments and a single pore domain (Kv1.2, Kv1.5, Kv2.1, Kv3.1, Kv3.3, Kv4.2 and Kv9.3) are reversibly blocked by hypoxia when expressed in heterologous expression systems. Additionally, the background K z channel subunit TASK-1, which comprises four transmembrane segments and two pore domains, is also involved in both oxygen-and acid-sensing in peripheral chemoreceptors.Progress is currently being made to identify the oxygen sensors. Regulatory b subunits may play an important role in the modulation of Kv channel subunits by oxygen.

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Section: Molecular Diversity Of Potassium Channels B Subunitsmentioning

confidence: 99%

Section: Molecular Diversity Of Potassium Channels B Subunitsmentioning

confidence: 99%

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Molecular physiology of oxygen-sensitive potassium channels

2001

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“…Immunolabeling was carried out, in part, as previously described (4). Cells attached onto poly-L-lysine-coated coverslips were washed with PBS and fixed with 4% paraformaldehyde for 20 min.…”

Section: Cells and Transfection Cd3mentioning

confidence: 99%

The Ca²⁺-activated K⁺ channel KCa3.1 compartmentalizes in the immunological synapse of human T lymphocytes

Nicolaou¹,

Neumeier²,

Peng³

et al. 2007

American Journal of Physiology-Cell Physiology

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T cell receptor engagement results in the reorganization of intracellular and membrane proteins at the T cell-antigen presenting cell interface forming the immunological synapse (IS), an event required for Ca2+ influx. KCa3.1 channels modulate Ca2+ signaling in activated T cells by regulating the membrane potential. Nothing is known regarding KCa3.1 membrane distribution during T cell activation. Herein, we determined whether KCa3.1 translocates to the IS in human T cells using YFP-tagged KCa3.1 channels. These channels showed electrophysiological and pharmacological properties identical to wild-type channels. IS formation was induced by either anti-CD3/CD28 antibody-coated beads for fixed microscopy experiments or Epstein-Barr virus-infected B cells for fixed and live cell microscopy. In fixed microscopy experiments, T cells were also immunolabeled for F-actin or CD3ε, which served as IS formation markers. The distribution of KCa3.1 was determined with confocal and fluorescence microscopy. We found that, upon T cell activation, KCa3.1 channels localize with F-actin and CD3ε to the IS but remain evenly distributed on the cell membrane when no stimulus is provided. Detailed imaging experiments indicated that KCa3.1 channels are recruited in the IS shortly after antigen presentation and are maintained there for at least 15–30 min. Interestingly, pretreatment of activated T cells with the specific KCa3.1 blocker TRAM-34 blocked Ca2+ influx, but channel redistribution to the IS was not prevented. These results indicate that KCa3.1 channels are a part of the signaling complex that forms at the IS upon antigen presentation.

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“…The complexity is further enhanced by the fact that the association of auxiliary subunits and interacting proteins also changes channel properties. Yet, determination of the molecular constituents of the native K O2 is an issue of capital importance to understand the molecular mechanisms of O 2 detection in chemoreceptor cells, to establish their physiological role in the native tissues, and additionally to provide a physiological meaning to the reported O 2 modulation of cloned channels expressed in heterologous systems (Hulme, J. T. et al 1999;Perez-Garcia, M. T. et al 1999;Conforti, L. et a l. 2000).…”

Section: Introductionmentioning

confidence: 99%

Oxygen sensitive Kv channels in the carotid body

López‐López

Pérez-Garcı́a

2007

Respiratory Physiology & Neurobiology

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Hypoxic inhibition of K+ channels has been documented in many native chemoreceptor cells, and is crucial to initiate reflexes directed to improve tissue O2 supply. In the carotid body (CB) chemoreceptors, it is a general consensus regarding the facts that a decrease in pO2 leads to membrane depolarization, increase of Ca2+ entry trough voltage-dependent Ca2+ channels and Ca2+-dependent release of neurotransmitters. Central to this pathway is the modulation by hypoxia of K+ channels that triggers depolarization. However, the details of this process are still controversial, and even the molecular nature of these oxygen-sensitive K+ (KO2) channels in the CB is hotly debated. Clearly there are inter-species differences, and even in the same preparation more that one KO2 may be present. Here we recapitulate our present knowledge of the role of voltage dependent K+ channels as KO2 in the CB from different species, and their functional contribution to cell excitability in response to acute and chronic exposure to hypoxia. Dear Dr Scheid:We have been very pleased to accept Drs. Kumar and Prabhakar invitation to contribute to a Special Issue on the physiology an pathophysiology of the carotid body. Following their instructions, we have written a review paper focused on the role of voltagedependent potassium channels as oxygen-modulated ion channels in the carotid body. We have tried to make an up to date account of all the data available in the literature to provide an overview of our knowledge regarding the presence, the molecular and functional characterization and the role in oxygen chemotransduction in the carotid body of these channels.This review is an original work that has not been published elsewhere, co-authored by Dr. J.R. López-López and myself. AbstractHypoxic inhibition of K + channels has been documented in many native chemoreceptor cells, and is crucial to initiate reflexes directed to improve tissue O 2 supply. In the carotid body (CB) chemoreceptors, it is a general consensus regarding the facts that a decrease in pO 2 leads to membrane depolarization, increase of Ca 2+ entry trough voltage-dependent Ca 2+ channels and Ca 2+ -dependent release of neurotransmitters. Central to this pathway is the modulation by hypoxia of K + channels that triggers depolarization. However, the details of this process are still controversial, and even the molecular nature of these oxygen-sensitive K + (K O2 ) channels in the CB is hotly debated. Clearly there are inter-species differences, and even in the same preparation more that one K O2 may be present. Here we recapitulate our present knowledge of the role of voltage dependent K + channels as K O2 in the CB from different species, and their functional contribution to cell excitability in response to acute and chronic exposure to hypoxia.

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O₂‐sensitive K⁺ channels: role of the Kv1.2 α‐subunit in mediating the hypoxic response

Cited by 93 publications

References 45 publications

Molecular physiology of oxygen-sensitive potassium channels

Molecular physiology of oxygen-sensitive potassium channels

The Ca²⁺-activated K⁺ channel KCa3.1 compartmentalizes in the immunological synapse of human T lymphocytes

Oxygen sensitive Kv channels in the carotid body

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O2‐sensitive K+ channels: role of the Kv1.2 α‐subunit in mediating the hypoxic response

Cited by 93 publications

References 45 publications

Molecular physiology of oxygen-sensitive potassium channels

Molecular physiology of oxygen-sensitive potassium channels

The Ca2+-activated K+ channel KCa3.1 compartmentalizes in the immunological synapse of human T lymphocytes

Oxygen sensitive Kv channels in the carotid body

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Resources

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O₂‐sensitive K⁺ channels: role of the Kv1.2 α‐subunit in mediating the hypoxic response

The Ca²⁺-activated K⁺ channel KCa3.1 compartmentalizes in the immunological synapse of human T lymphocytes