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AMP-activated protein kinase and chemotransduction in the carotid body

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AMP-activated protein kinase and chemotransduction in the carotid body. / Wyatt, Christopher N.; Evans, A. Mark.

In: Respiratory Physiology & Neurobiology, Vol. 157, 01.07.2007, p. 22-29.

Research output: Contribution to journalArticle

Harvard

Wyatt, CN & Evans, AM 2007, 'AMP-activated protein kinase and chemotransduction in the carotid body', Respiratory Physiology & Neurobiology, vol. 157, pp. 22-29. https://doi.org/10.1016/j.resp.2007.01.021

APA

Wyatt, C. N., & Evans, A. M. (2007). AMP-activated protein kinase and chemotransduction in the carotid body. Respiratory Physiology & Neurobiology, 157, 22-29. https://doi.org/10.1016/j.resp.2007.01.021

Vancouver

Wyatt CN, Evans AM. AMP-activated protein kinase and chemotransduction in the carotid body. Respiratory Physiology & Neurobiology. 2007 Jul 1;157:22-29. https://doi.org/10.1016/j.resp.2007.01.021

Author

Wyatt, Christopher N. ; Evans, A. Mark. / AMP-activated protein kinase and chemotransduction in the carotid body. In: Respiratory Physiology & Neurobiology. 2007 ; Vol. 157. pp. 22-29.

Bibtex - Download

@article{68acdc43f45f4355a192ea358ea0bb4f,
title = "AMP-activated protein kinase and chemotransduction in the carotid body",
abstract = "AMP-activated protein kinase (AMPK) is a key component of a kinase cascade that regulates energy balance at the cellular level. Our recent research has raised the possibility that AMPK may also function to couple hypoxic inhibition of mitochondrial oxidative phosphorylation to O-2-sensitive K+ channel inhibition and hence underpin carotid body type I cell excitation. Thus, in addition to maintaining the cellular energy state AMPK may act as the primary metabolic sensor and effector of hypoxic chemotransduction in type I cells. These findings provide a unifying link between two previously separate theories pertaining to O-2-sensing in the carotid body, namely the 'membrane hypothesis' and the 'mitochondrial hypothesis'. Furthermore, our data suggest that in addition to its effects at the cellular level the AMPK signalling cascade can mediate vital physiological mechanisms essential for meeting the metabolic needs of the whole organism. (c) 2007 Elsevier B.V. All rights reserved.",
keywords = "hypoxic chemotransduction, carotid body, AMP-activated protein kinase, MITOCHONDRIAL OXIDATIVE-PHOSPHORYLATION, HYPOXIA-INDUCIBLE FACTOR-1-ALPHA, ARTERIAL CHEMORECEPTOR CELLS, CHRONIC INTERMITTENT HYPOXIA, I CELLS, GLOMUS CELLS, POTASSIUM CHANNEL, OXYGEN SENSOR, K+ CURRENT, TRANSCRIPTIONAL ACTIVITY",
author = "Wyatt, {Christopher N.} and Evans, {A. Mark}",
year = "2007",
month = "7",
day = "1",
doi = "10.1016/j.resp.2007.01.021",
language = "English",
volume = "157",
pages = "22--29",
journal = "Respiratory Physiology & Neurobiology",
issn = "1569-9048",
publisher = "Elsevier",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - AMP-activated protein kinase and chemotransduction in the carotid body

AU - Wyatt, Christopher N.

AU - Evans, A. Mark

PY - 2007/7/1

Y1 - 2007/7/1

N2 - AMP-activated protein kinase (AMPK) is a key component of a kinase cascade that regulates energy balance at the cellular level. Our recent research has raised the possibility that AMPK may also function to couple hypoxic inhibition of mitochondrial oxidative phosphorylation to O-2-sensitive K+ channel inhibition and hence underpin carotid body type I cell excitation. Thus, in addition to maintaining the cellular energy state AMPK may act as the primary metabolic sensor and effector of hypoxic chemotransduction in type I cells. These findings provide a unifying link between two previously separate theories pertaining to O-2-sensing in the carotid body, namely the 'membrane hypothesis' and the 'mitochondrial hypothesis'. Furthermore, our data suggest that in addition to its effects at the cellular level the AMPK signalling cascade can mediate vital physiological mechanisms essential for meeting the metabolic needs of the whole organism. (c) 2007 Elsevier B.V. All rights reserved.

AB - AMP-activated protein kinase (AMPK) is a key component of a kinase cascade that regulates energy balance at the cellular level. Our recent research has raised the possibility that AMPK may also function to couple hypoxic inhibition of mitochondrial oxidative phosphorylation to O-2-sensitive K+ channel inhibition and hence underpin carotid body type I cell excitation. Thus, in addition to maintaining the cellular energy state AMPK may act as the primary metabolic sensor and effector of hypoxic chemotransduction in type I cells. These findings provide a unifying link between two previously separate theories pertaining to O-2-sensing in the carotid body, namely the 'membrane hypothesis' and the 'mitochondrial hypothesis'. Furthermore, our data suggest that in addition to its effects at the cellular level the AMPK signalling cascade can mediate vital physiological mechanisms essential for meeting the metabolic needs of the whole organism. (c) 2007 Elsevier B.V. All rights reserved.

KW - hypoxic chemotransduction

KW - carotid body

KW - AMP-activated protein kinase

KW - MITOCHONDRIAL OXIDATIVE-PHOSPHORYLATION

KW - HYPOXIA-INDUCIBLE FACTOR-1-ALPHA

KW - ARTERIAL CHEMORECEPTOR CELLS

KW - CHRONIC INTERMITTENT HYPOXIA

KW - I CELLS

KW - GLOMUS CELLS

KW - POTASSIUM CHANNEL

KW - OXYGEN SENSOR

KW - K+ CURRENT

KW - TRANSCRIPTIONAL ACTIVITY

UR - http://www.scopus.com/inward/record.url?scp=34247260003&partnerID=8YFLogxK

U2 - 10.1016/j.resp.2007.01.021

DO - 10.1016/j.resp.2007.01.021

M3 - Article

VL - 157

SP - 22

EP - 29

JO - Respiratory Physiology & Neurobiology

JF - Respiratory Physiology & Neurobiology

SN - 1569-9048

ER -

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