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
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
Combined Automated Annotation using Multiple IEA Methods
Intracellular trafficking of the JNCL protein CLN3.
Studies of membrane association of CLN3 protein.
Tissue expression and subcellular localization of CLN3, the Batten disease protein.
Defective intracellular transport of CLN3 is the molecular basis of Batten disease (JNCL).
CLN3 protein regulates lysosomal pH and alters intracellular processing of Alzheimer's amyloid-beta protein precursor and cathepsin D in human cells.
CLN3 protein is targeted to neuronal synapses but excluded from synaptic vesicles: new clues to Batten disease.
Elevated lysosomal pH in neuronal ceroid lipofuscinoses (NCLs).
Neuronal ceroid lipofuscinoses are connected at molecular level: interaction of CLN5 protein with CLN2 and CLN3.
Membrane topology of CLN3, the protein underlying Batten disease.
Intracellular trafficking of CLN3, the protein underlying the childhood neurodegenerative disease, Batten disease.
Two motifs target Batten disease protein CLN3 to lysosomes in transfected nonneuronal and neuronal cells.
A galactosylceramide binding domain is involved in trafficking of CLN3 from Golgi to rafts via recycling endosomes.
Interconnections of CLN3, Hook1 and Rab proteins link Batten disease to defects in the endocytic pathway.
AP-1 and AP-3 facilitate lysosomal targeting of Batten disease protein CLN3 via its dileucine motif.
Defective lysosomal arginine transport in juvenile Batten disease.
Neuronal vulnerability of CLN3 deletion to calcium-induced cytotoxicity is mediated by calsenilin.
Neuronal ceroid lipofuscinosis: a common pathway?
C-terminal prenylation of the CLN3 membrane glycoprotein is required for efficient endosomal sorting to lysosomes.
A novel role of the Batten disease gene CLN3: association with BMP synthesis.
Integral and associated lysosomal membrane proteins.
CLN3p impacts galactosylceramide transport, raft morphology, and lipid content.
Loss of the Batten disease gene CLN3 prevents exit from the TGN of the mannose 6-phosphate receptor.
Novel interactions of CLN5 support molecular networking between Neuronal Ceroid Lipofuscinosis proteins.
Interaction between Sdo1p and Btn1p in the Saccharomyces cerevisiae model for Batten disease.
A novel interaction of CLN3 with nonmuscle myosin-IIB and defects in cell motility of Cln3(-/-) cells.
Neuronal ceroid lipofuscinosis protein CLN3 interacts with motor proteins and modifies location of late endosomal compartments.
Osmotic stress changes the expression and subcellular localization of the Batten disease protein CLN3.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Biosynthesis and intracellular targeting of the CLN3 protein defective in Batten disease.
The Batten disease gene product (CLN3p) is a Golgi integral membrane protein.
CLN3 transports GalCer to plasma membrane
Glycosphingolipid transport
CLN3 mediates chloride efflux from lysosomes.
CLN3 is required for the clearance of glycerophosphodiesters from lysosomes.
Glycerophosphodiesters inhibit lysosomal phospholipid catabolism in Batten disease.
Membrane trafficking and mitochondrial abnormalities precede subunit c deposition in a cerebellar cell model of juvenile neuronal ceroid lipofuscinosis.
Autophagy is disrupted in a knock-in mouse model of juvenile neuronal ceroid lipofuscinosis.
Osmoregulation of ceroid neuronal lipofuscinosis type 3 in the renal medulla.
CLN3 loss disturbs membrane microdomain properties and protein transport in brain endothelial cells.
Defective synaptic transmission causes disease signs in a mouse model of juvenile neuronal ceroid lipofuscinosis.
Photoreceptor phagosome processing defects and disturbed autophagy in retinal pigment epithelium of Cln3Δex1-6 mice modelling juvenile neuronal ceroid lipofuscinosis (Batten disease).
Altered Cerebellar Short-Term Plasticity but No Change in Postsynaptic AMPA-Type Glutamate Receptors in a Mouse Model of Juvenile Batten Disease.
CLN3 source and assay provenance
Selected original CLN3 primary passage