Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor

Stephen J. Tucker, Fiona M. Gribble, Chao Zhao, Stefan Trapp and Frances M. Ashcroft
Additional contact information
Stephen J. Tucker: University Laboratory of Physiology
Fiona M. Gribble: University Laboratory of Physiology
Chao Zhao: University Laboratory of Physiology
Stefan Trapp: University Laboratory of Physiology
Frances M. Ashcroft: University Laboratory of Physiology

Nature, 1997, vol. 387, issue 6629, 179-183

Abstract: Abstract ATP-sensitive potassium channels (K-ATP channels) couple cell metabolism to electrical activity and are important in the physiology and pathophysiology of many tissues1. In pancreatic β-cells, K-ATP channels link changes in blood glucose concentration to insulin secretion2. They are also the target for clinically important drugs such as sulphonylureas, which stimulate secretion, and the K+ channel opener diazoxide, which inhibits insulin release3,4. Metabolic regulation of K-ATP channels is mediated by changes in intracellular ATP and Mg-ADP levels, which inhibit and activate the channel, respectively2. The β-cell K-ATP channel is a complex of two proteins5,6: an inward-rectifier K+ channel subunit, Kir6.2, and the sulphonylurea receptor, SUR1. We show here that the primary site at which ATP acts to mediate K-ATP channel inhibition is located on Kir6.2, and that SUR1 is required for sensitivity to sulphonylureas and diazoxide and for activation by Mg-ADP.

Date: 1997
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/387179a0 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:387:y:1997:i:6629:d:10.1038_387179a0

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/387179a0

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().