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- W2055754237 abstract "Activating mutations in different domains of the ABCC8 gene-coded sulfonylurea receptor 1 (SUR1) cause neonatal diabetes. Here we show that a diabetogenic mutation in an unexplored helix preceding the ABC core of SUR1 dramatically increases open probability of (SUR1/Kir6.2)(4) channel (KATP) by reciprocally changing rates of its transitions to and from the long-lived, inhibitory ligand-stabilized closed state. This kinetic mechanism attenuates ATP and sulfonylurea inhibition, but not Mg-nucleotide stimulation, of SUR1/Kir6.2. The results suggest a key role for L0 helix in KATP gating and together with previous findings from mutant KATP clarify why many patients with neonatal diabetes require high doses of sulfonylureas." @default.
- W2055754237 created "2016-06-24" @default.
- W2055754237 creator A5039077702 @default.
- W2055754237 creator A5064513248 @default.
- W2055754237 date "2011-10-19" @default.
- W2055754237 modified "2023-09-23" @default.
- W2055754237 title "Mechanism of KATP hyperactivity and sulfonylurea tolerance due to a diabetogenic mutation in L0 helix of sulfonylurea receptor 1 (ABCC8)" @default.
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- W2055754237 doi "https://doi.org/10.1016/j.febslet.2011.10.020" @default.
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