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Intrinsic sensitivity of Kir1.1 (ROMK) to glibenclamide in the absence of SUR2B. Implications for the identity of the renal ATP-regulated secretory K+ channel.

Abstract:

The precise molecular identity of the renal ATP-regulated secretory K+ channel is still a matter of some controversy. The inwardly rectifying K+ channel, Kir1.1 (ROMK) appears to form the pore of the channel, and mutations in Kir1.1 are responsible for Bartter syndrome. The native channel is sensitive to inhibition by the sulfonylurea glibenclamide, and it has been proposed that an accessory protein is required to confer glibenclamide sensitivity to Kir1.1. Several recent studies have suggest...

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Publication status:
Published

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Publisher copy:
10.1074/jbc.m202005200

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Institution:
University of Oxford
Division:
MPLS
Department:
Physics
Sub department:
Condensed Matter Physics
Role:
Author
Journal:
Journal of biological chemistry
Volume:
277
Issue:
24
Pages:
21346-21351
Publication date:
2002-06-01
DOI:
EISSN:
1083-351X
ISSN:
0021-9258
Source identifiers:
22481

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