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.

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 sensiti...

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Những tác giả chính: Konstas, A, Dabrowski, M, Korbmacher, C, Tucker, S
Định dạng: Journal article
Ngôn ngữ:English
Được phát hành: 2002