Associated Papers
Multilocus Disease-Causing Genomic Variations for Genetic Disorders: Single Tertiary Centre Experience From Türkiye.
Kablan A et al.
Clinical Genetics, 2025
Structure of an open KATP channel reveals tandem PIP2 binding sites mediating the Kir6.2 and SUR1 regulatory interface.
Driggers CM et al.
Nature Communications, 2024
Structure of an open K ATP channel reveals tandem PIP 2 binding sites mediating the Kir6.2 and SUR1 regulatory interface.
Driggers CM et al.
Biorxiv : the Preprint Server for Biology, 2024
Statistical evidence for high-penetrance MODY-causing genes in a large population-based cohort.
Billings LK et al.
Endocrinology, Diabetes & Metabolism, 2022
36208030 (PubMed )
Supplement: EDM2-5-e372-s001.xlsx › eTable_1
Determinants of trafficking, conduction, and disease within a K+ channel revealed through multiparametric deep mutational scanning.
Coyote-Maestas W et al.
Elife, 2022
35639599 (PubMed )
Supplement: elife-76903-data1.zip › SourceData › input_data › KCNJ_Clinvar_0325322_edited_annotations_.xlsx › clinvar_KCNJx_0325322
Update of variants identified in the pancreatic β-cell KATP channel genes KCNJ11 and ABCC8 in individuals with congenital hyperinsulinism and diabetes.
De Franco E et al.
Human Mutation, 2020
ATP-sensitive K+ channels: regulation of bursting by the sulphonylurea receptor, PIP2 and regions of Kir6.2.
Ribalet B et al.
The Journal of Physiology, 2006
ATP sensitivity of ATP-sensitive K+ channels: role of the gamma phosphate group of ATP and the R50 residue of mouse Kir6.2.
John SA et al.
The Journal of Physiology, 2005
Identification of residues contributing to the ATP binding site of Kir6.2.
Trapp S et al.
The Embo Journal, 2003
Molecular basis for Kir6.2 channel inhibition by adenine nucleotides.
Ribalet B et al.
Biophysical Journal, 2003
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