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Toward linking structure with function in ATP-sensitive K+ channels Bryan J; Vila-Carriles WH; Zhao G; Babenko AP; Aguilar-Bryan LDiabetes 2004[Dec]; 53 Suppl 3 (ä): S104-12Advances in understanding the overall structural features of inward rectifiers and ATP-binding cassette (ABC) transporters are providing novel insight into the architecture of ATP-sensitive K+ channels (KATP channels) (KIR6.0/SUR)4. The structure of the K(IR) pore has been modeled on bacterial K+ channels, while the lipid-A exporter, MsbA, provides a template for the MDR-like core of sulfonylurea receptor (SUR)-1. TMD0, an NH2-terminal bundle of five alpha-helices found in SURs, binds to and activates KIR6.0. The adjacent cytoplasmic L0 linker serves a dual function, acting as a tether to link the MDR-like core to the KIR6.2/TMD0 complex and exerting bidirectional control over channel gating via interactions with the NH2-terminus of the KIR. Homology modeling of the SUR1 core offers the possibility of defining the glibenclamide/sulfonylurea binding pocket. Consistent with 30-year-old studies on the pharmacology of hypoglycemic agents, the pocket is bipartite. Elements of the COOH-terminal half of the core recognize a hydrophobic group in glibenclamide, adjacent to the sulfonylurea moiety, to provide selectivity for SUR1, while the benzamido group appears to be in proximity to L0 and the KIR NH2-terminus.|ATP-Binding Cassette Transporters/metabolism[MESH]|Adenosine Triphosphate/*physiology[MESH]|Animals[MESH]|Humans[MESH]|Hypoglycemic Agents/pharmacology[MESH]|Models, Molecular[MESH]|Potassium Channels, Inwardly Rectifying/chemistry/drug effects/physiology[MESH]|Potassium Channels/*chemistry/drug effects/*physiology[MESH]|Protein Conformation[MESH] |
