Acute hypoxic regulation of recombinant THIK-1 stably expressed in HEK293 cells
Fearon, Ian M., Campanucci, Veronica A., Brown, Stephen T., Hudasek, Kristin, O'Kelly, Ita M. and Nurse, Colin A. (2006) Acute hypoxic regulation of recombinant THIK-1 stably expressed in HEK293 cells In, The Arterial Chemoreceptors. USA, Springer pp. 203-208. (Advances in Experimental Medicine and Biology, 580). (doi:10.1007/0-387-31311-7_31).
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Hypoxic inhibition of O2-sensitive K+ channels plays a key role in mediating numerous cellular responses which counteract the deleterious effects of hypoxia. In type I cells of the carotid body (CB), a neurosecretory organ that responds to hypoxia by releasing neurotransmitters from specialized O2-sensing type I cells onto sensory nerve endings, hypoxic inhibition of K+ channels underlies the membrane depolarisation (Lopez-Barneo et al., 1988) that stimulates Ca2+ entry and neurotransmitter release (Urena et al., 1994). In other neurosecretory cells, such as those located in the neuroepithelial cell bodies of the lung (Youngson et al., 1993) and the adrenal medulla (Thompson and Nurse, 1998), hypoxic inhibition of K+ channels provides a critical link between O2 levels and the appropriate cellular responses.
|Item Type:||Book Section|
|Digital Object Identifier (DOI):||doi:10.1007/0-387-31311-7_31|
|Keywords:||protein, tandem pore domain, recombinant proteins, human, cell hypoxia, genetics, physiology, proteins, potassium channels, metabolism, research, gene expression regulation, cell line|
|Date Deposited:||08 Sep 2008|
|Last Modified:||16 Apr 2017 17:33|
|Further Information:||Google Scholar|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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