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

Combined Automated Annotation using Multiple IEA Methods

Mutations in SPG11, encoding spatacsin, are a major cause of spastic paraplegia with thin corpus callosum.

Integral and associated lysosomal membrane proteins.

A genome-scale DNA repair RNAi screen identifies SPG48 as a novel gene associated with hereditary spastic paraplegia.

Cellular distribution and subcellular localization of spatacsin and spastizin, two proteins involved in hereditary spastic paraplegia.

Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.

Dysfunction of spatacsin leads to axonal pathology in SPG11-linked hereditary spastic paraplegia.

Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation.

A proteome-scale map of the human interactome network.

Inhibition of Lysosome Membrane Recycling Causes Accumulation of Gangliosides that Contribute to Neurodegeneration.

Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.

Cytosolic sequestration of spatacsin by Protein Kinase A and 14-3-3 proteins.

Spatacsin regulates directionality of lysosome trafficking by promoting the degradation of its partner AP5Z1.

Structural basis for membrane remodeling by the AP5-SPG11-SPG15 complex.