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Cloning of the human TASK-2 (KCNK5) promoter and its regulation by chronic hypoxia

Brazier, Stephen P., Mason, Helen S., Bateson, Alan N. and Kemp, Paul J. 2005. Cloning of the human TASK-2 (KCNK5) promoter and its regulation by chronic hypoxia. Biochemical and Biophysical Research Communications 336 (4) , pp. 1251-1258. 10.1016/j.bbrc.2005.09.007

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Abstract

The tandem P domain potassium channel family includes five members of the acid-sensing subfamily, TASK. TASK channels are active at resting potential and are inhibited by extracellular protons, suggesting they function as acid sensors and control excitability/ion homeostasis. Indeed, TASK-2 (KCNK5) has been shown to control excitability, volume regulation, bicarbonate handling, and apoptosis in a variety of tissues. With such diverse functions being ascribed to TASK-2, it is important to understand long-term as well as short-term regulation of this important channel. Thus, we have cloned the TASK-2 promoter, demonstrated that its transcriptional activity is dependent upon pO2, shown that deletion of overlapping consensus binding sites for NF-κB/Elk-1 ablates this O2 sensitivity, and proved that Elk-1 binds preferentially to this site. Furthermore, the consequences of chronic hypoxia on natively expressed TASK-2 are decreased steady-state mRNA and cell depolarization showing that TASK-2 contributes to the excitability of this important lung cell type.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: Elsevier
ISSN: 0006-291X
Last Modified: 04 Jun 2017 06:39
URI: http://orca-mwe.cf.ac.uk/id/eprint/63406

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