Gene Ontology annotation through association of InterPro records with GO terms
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
Electronic Gene Ontology annotations created by ARBA machine learning models
AP-4, a novel protein complex related to clathrin adaptors.
Characterization of a fourth adaptor-related protein complex.
Similar subunit interactions contribute to assembly of clathrin adaptor complexes and COPI complex: analysis using yeast three-hybrid system.
Functional and physical interactions of the adaptor protein complex AP-4 with ADP-ribosylation factors (ARFs).
AP-4 binds basolateral signals and participates in basolateral sorting in epithelial MDCK cells.
Recognition of dileucine-based sorting signals from HIV-1 Nef and LIMP-II by the AP-1 gamma-sigma1 and AP-3 delta-sigma3 hemicomplexes.
Sorting of the Alzheimer's disease amyloid precursor protein mediated by the AP-4 complex.
Conservation and diversification of dileucine signal recognition by adaptor protein (AP) complex variants.
Adaptor protein complex 4 deficiency causes severe autosomal-recessive intellectual disability, progressive spastic paraplegia, shy character, and short stature.
Structural and functional characterization of cargo-binding sites on the μ4-subunit of adaptor protein complex 4.
Recessive loss-of-function mutations in AP4S1 cause mild fever-sensitive seizures, developmental delay and spastic paraplegia through loss of AP-4 complex assembly.
AP-4 vesicles contribute to spatial control of autophagy via RUSC-dependent peripheral delivery of ATG9A.
Axonal autophagosome maturation defect through failure of ATG9A sorting underpins pathology in AP-4 deficiency syndrome.
Utilizing RNA and outlier analysis to identify an intronic splice-altering variant in AP4S1 in a sibling pair with progressive spastic paraplegia.
Adaptor protein complex 4 deficiency: a paradigm of childhood-onset hereditary spastic paraplegia caused by defective protein trafficking.
Loss of ap4s1 in zebrafish leads to neurodevelopmental defects resembling spastic paraplegia 52.
Defining the clinical, molecular and imaging spectrum of adaptor protein complex 4-associated hereditary spastic paraplegia.
High-throughput imaging of ATG9A distribution as a diagnostic functional assay for adaptor protein complex 4-associated hereditary spastic paraplegia.
The adaptor protein chaperone AAGAB stabilizes AP-4 complex subunits.
Ap4s1 truncation leads to axonal defects in a zebrafish model of spastic paraplegia 52.
Heterozygous variants in AP4S1 are not associated with a neurological phenotype.
Uncovering cargo clients and accessory factors of AP-1 and AP-4 through vesicle proteomics.
Structural basis for the dynamic conformations of AP-4 and its association with ARF1.
AP4 transports APP from trans-Golgi network to endosome lumen
AP4S1 (sigma4): is the large-subunit half of the dileucine basic patch present in AP-4 epsilon?
Affinage mechanistic annotation for AP4S1 (human)
UniProtKB Q9Y587 (AP4S1_HUMAN) flat file