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
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
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
Molecular mechanism for ATP-dependent closure of the K+ channel Kir6.2.
Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.
Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.
The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy.
ATP-sensitive K+ channels in pig urethral smooth muscle cells are heteromultimers of Kir6.1 and Kir6.2.
Dual role of K ATP channel C-terminal motif in membrane targeting and metabolic regulation.
Ankyrin-B regulates Kir6.2 membrane expression and function in heart.
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.
A reference map of the human binary protein interactome.
Mutation of the pancreatic islet inward rectifier Kir6.2 also leads to familial persistent hyperinsulinemic hypoglycemia of infancy.
Activation of ATP sensitive Potassium channels in neuroendocrine cells
Activation of ATP sensitive Potassium channels in muscle cells
KCNJ11 tetramer:ABCC8 tetramer binds 4xATP, closing the channel
KCNJ11:ABCC9 transports K+ from extracellular region to cytosol
Defective ABCC9 (in KCNJ11:ABCC9) does not transport K+ from extracellular region to cytosol
Defective ABCC8 does not form functional KATP channels, causing hyperinsulinemic hypoglycemia
SU drugs bind ABCC8 (in KCNJ11 tetramer:ABCC8:Mg2+:ADP tetramer)
KCNJ11:ABCC9 binds nicorandil
Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor.