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
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
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
Electronic Gene Ontology annotations created by ARBA machine learning models
Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death.
A cardiac arrhythmia syndrome caused by loss of ankyrin-B function.
Ankyrin-B targets beta2-spectrin to an intracellular compartment in neonatal cardiomyocytes.
The ammonium transporter RhBG: requirement of a tyrosine-based signal and ankyrin-G for basolateral targeting and membrane anchorage in polarized kidney epithelial cells.
Targeting and stability of Na/Ca exchanger 1 in cardiomyocytes requires direct interaction with the membrane adaptor ankyrin-B.
Defining the cellular phenotype of "ankyrin-B syndrome" variants: human ANK2 variants associated with clinical phenotypes display a spectrum of activities in cardiomyocytes.
Systematic identification of SH3 domain-mediated human protein-protein interactions by peptide array target screening.
Obscurin targets ankyrin-B and protein phosphatase 2A to the cardiac M-line.
Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease.
Ankyrin-B is required for coordinated expression of beta-2-spectrin, the Na/K-ATPase and the Na/Ca exchanger in the inner segment of rod photoreceptors.
Ankyrin-based targeting pathway regulates human sinoatrial node automaticity.
An ankyrin-based mechanism for functional organization of dystrophin and dystroglycan.
Dual role of K ATP channel C-terminal motif in membrane targeting and metabolic regulation.
EH domain proteins regulate cardiac membrane protein targeting.
Ankyrin-B regulates Kir6.2 membrane expression and function in heart.
Asparagine and aspartate hydroxylation of the cytoskeletal ankyrin family is catalyzed by factor-inhibiting hypoxia-inducible factor.
Defects in ankyrin-based membrane protein targeting pathways underlie atrial fibrillation.
CK2-regulated schwannomin-interacting protein IQCJ-SCHIP-1 association with AnkG contributes to the maintenance of the axon initial segment.
Identification of Human Neuronal Protein Complexes Reveals Biochemical Activities and Convergent Mechanisms of Action in Autism Spectrum Disorders.
Histone Interaction Landscapes Visualized by Crosslinking Mass Spectrometry in Intact Cell Nuclei.
Structural Basis Underlying Strong Interactions between Ankyrins and Spectrins.
Protein interaction studies in human induced neurons indicate convergent biology underlying autism spectrum disorders.
L1 linked to actin cytoskeleton by ankyrin
Phosphorylation of Y1229 in L1
ARFGAP, cargo, v-SNAREs and p24 proteins bind nascent COPI complex
ARFGAPs stimulate ARF GTPase activity
ERGIC-to-Golgi vesicles bind dynein:dynactin
Vesicle is tethered through binding GOLGA2:GORASP1, GOLGB1 and the COG complex
cis-Golgi t-SNAREs bind YKT6 on tethered vesicle
Selective disappearance of an axonal protein, 440-kDa ankyrinB, associated with neuronal degeneration induced by methylmercury.
Glial ankyrins facilitate paranodal axoglial junction assembly.
A PIK3C3-ankyrin-B-dynactin pathway promotes axonal growth and multiorganelle transport.
Ankyrin-B is a PI3P effector that promotes polarized α5β1-integrin recycling via recruiting RabGAP1L to early endosomes.
Giant ankyrin-B suppresses stochastic collateral axon branching through direct interaction with microtubules.
Giant ankyrin-B mediates transduction of axon guidance and collateral branch pruning factor sema 3A.