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siRNA knock-down of γ-glutamyl transpeptidase does not affect hypoxic K+ channel inhibition

Williams, Sandile E., Wootton, Phillippa, Mason, Helen S., Iles, David E., Peers, C. and Kemp, Paul J. 2004. siRNA knock-down of γ-glutamyl transpeptidase does not affect hypoxic K+ channel inhibition. Biochemical and Biophysical Research Communications 314 (1) , pp. 63-68. 10.1016/j.bbrc.2003.12.052

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Large conductance, Ca2+-sensitive potassium (BK) channels are critical components of the O2 signalling cascade in a number of cells, including the carotid body and central neurones. Although the nature of the BK channel O2 sensor is still unknown, evidence suggests redox modulators might form part of the O2 sensing channel complex. By metabolising glutathione, γ-glutamyl transpeptidase (γGT) could act as such an O2 sensor. Western blotting and immunocytochemistry revealed high γGT expression in HEK293 cells expressing the α- and β-subunits of human recombinant BK and γGT co-immunoprecipitated with BKα. Acivicin blockade of γGT reversibly inhibited BK channels, suggesting that this BKα protein partner contributes to tonic channel activity. However, knock-out of γGT using siRNA had no effect on hypoxic BK channel inhibition. Together, these data indicate that γGT is a BKα protein partner, that its activity regulates BK channels but that it is not the BK O2 sensor.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: Elsevier
ISSN: 0006-291X
Last Modified: 04 Jun 2017 06:39

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