Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Manual transfer of experimentally-verified manual GO annotation data to homologous complexes by curator judgment of sequence, composition and function similarity
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Ankyrin-B regulates Kir6.2 membrane expression and function in heart.
Monoallelic ABCC8 mutations are a common cause of diazoxide-unresponsive diffuse form of congenital hyperinsulinism.
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Human disease variants distinguish normal membrane trafficking from failed MgADP/diazoxide activation.
"Seven of the 8 mutants reaching the plasma membrane had dramatically reduced response to MgADP or to diazoxide (<10% of wild-type response)."
Alternating hypoglycemia and hyperglycemia in a toddler with a homozygous p.R1419H ABCC8 mutation: an unusual clinical picture.
Molecular determinants of ATP-sensitive potassium channel MgATPase activity: diabetes risk variants and diazoxide sensitivity.
Conserved functional consequences of disease-associated mutations in the slide helix of Kir6.1 and Kir6.2 subunits of the ATP-sensitive potassium channel.
Molecular structure of human KATP in complex with ATP and ADP.
Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor.
Activation of ATP sensitive Potassium channels in neuroendocrine cells
KCNJ11 tetramer:ABCC8 tetramer binds 4xATP, closing the channel
Regulation of insulin secretion
Defective ABCC8 does not form functional KATP channels, causing hyperinsulinemic hypoglycemia
Activating ABCC8 mutants cause hyperglycemia in permanent neonatal diabetes mellitus (PNDM) and transient neonatal DM (TNDM)
SU drugs bind ABCC8 (in KCNJ11 tetramer:ABCC8:Mg2+:ADP tetramer)
Antihyperglycemic and antihyperlipidemic effects of newly synthesized glibenclamide analogues on streptozotocin-diabetic rats.
Ontogeny of sulfonylurea-binding regulatory subunits of K(ATP) channels in the pregnant rat myometrium.
ATP-sensitive potassium channels modulate in vitro tocolytic effects of β₂-adrenergic receptor agonists on uterine muscle rings in rats in early but not in late pregnancy.
Inhibition of the Sur1-Trpm4 channel reduces neuroinflammation and cognitive impairment in subarachnoid hemorrhage.
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Antisense and drug inhibition corroborate the injury-associated direction of SUR1 barrier signaling.
"inhibiting Sur1 using antisense or the selective Sur1 inhibitor glibenclamide reduced SAH-induced immunoglobulin G extravasation"
Two SUR1-specific histidine residues mandatory for zinc-induced activation of the rat KATP channel.
Risperidone reduces mRNA expression levels of Sulfonylurea Receptor 1 and TASK1 in PC12 cells.
Glibenclamide enhances neurogenesis and improves long-term functional recovery after transient focal cerebral ischemia.
Syntaxin-1A binds the nucleotide-binding folds of sulphonylurea receptor 1 to regulate the KATP channel.
Nitric oxide differentially regulates renal ATP-binding cassette transporters during endotoxemia.
Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage.
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SUR1 inhibition reduces barrier leakage, supporting a positive permeability role in the injury model.
"inhibiting SUR1 using low-dose glibenclamide after SAH resulted in a significant reduction in IgG extravasation"
Effects of caudal fourth ventricular lactate infusion on hypoglycemia-associated MCT2, GLUT3, GLUT4, GCK, and sulfonylurea receptor-1 gene expression in the ovariectomized female rat LHA and VMH: impact of estradiol.
Immunolocalization of KATP channel subunits in mouse and rat cardiac myocytes and the coronary vasculature.
Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.
Arylcyanoguanidines as activators of Kir6.2/SUR1K ATP channels and inhibitors of insulin release.
Inhibition of SUR1 decreases the vascular permeability of cerebral metastases.
Cryo-EM structure of the ATP-sensitive potassium channel illuminates mechanisms of assembly and gating.
The sulfonylurea receptor 1 (Sur1)-transient receptor potential melastatin 4 (Trpm4) channel.
On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1.
Molecular structure of an open human K(ATP) channel.
ATP binding without hydrolysis switches sulfonylurea receptor 1 (SUR1) to outward-facing conformations that activate K(ATP) channels.
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ATP binding can activate sensitized channels without requiring hydrolysis in every opening event.
"ATP binding to SUR1, without hydrolysis, opens channels when nucleotide antagonism on Kir6.2 is minimized"
ABCC8 functional-annotation research report (Falcon)
Hyperinsulinism in mice with heterozygous loss of K(ATP) channels.
Cryo-electron microscopy structures and progress toward a dynamic understanding of K(ATP) channels.
Mechanism of pharmacochaperoning in a mammalian K(ATP) channel revealed by cryo-EM.
Pharmacological chaperones of ATP-sensitive potassium channels: Mechanistic insight from cryoEM structures.
Personalized Therapeutics for K(ATP)-Dependent Pathologies.
The Changing Landscape of Neonatal Diabetes Mellitus in Italy Between 2003 and 2022.
Dynamic duo: Kir6 and SUR in K(ATP) channel structure and function.
Congenital Hyperinsulinism Caused by Mutations in ABCC8 Gene Associated with Early-Onset Neonatal Hypoglycemia: Genetic Heterogeneity Correlated with Phenotypic Variability.
Transient diabetes mellitus with ABCC8 variant successfully treated with sulfonylurea: Two case reports and review of literature.
Non-surgical Treatment May be Appropriate for Most Chinese Children With Monogenic Congenital Hyperinsulinism Based on a Retrospective Study of 121 Patients.