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

Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs

Combined Automated Annotation using Multiple IEA Methods

Localization of the murine Niemann-Pick C1 protein to two distinct intracellular compartments.

Topological analysis of Niemann-Pick C1 protein reveals that the membrane orientation of the putative sterol-sensing domain is identical to those of 3-hydroxy-3-methylglutaryl-CoA reductase and sterol regulatory element binding protein cleavage-activating protein.

Defective endocytic trafficking of NPC1 and NPC2 underlying infantile Niemann-Pick type C disease.

Genetic evidence for nonredundant functional cooperativity between NPC1 and NPC2 in lipid transport.

Accumulation of glycosphingolipids in Niemann-Pick C disease disrupts endosomal transport.

NPC2 is expressed in human and murine liver and secreted into bile: potential implications for body cholesterol homeostasis.

Cholesterol depletion facilitates ubiquitylation of NPC1 and its association with SKD1/Vps4.

Different cellular traffic of LDL-cholesterol and acetylated LDL-cholesterol leads to distinct reverse cholesterol transport pathways.

Autophagy in Niemann-Pick C disease is dependent upon Beclin-1 and responsive to lipid trafficking defects.

NPC2 facilitates bidirectional transfer of cholesterol between NPC1 and lipid bilayers, a step in cholesterol egress from lysosomes.

Tau deletion exacerbates the phenotype of Niemann-Pick type C mice and implicates autophagy in pathogenesis.

A molecular mechanism underlying the neural-specific defect in torsinA mutant mice.

Quantitative role of LAL, NPC2, and NPC1 in lysosomal cholesterol processing defined by genetic and pharmacological manipulations.

Unesterified cholesterol accumulation in late endosomes/lysosomes causes neurodegeneration and is prevented by driving cholesterol export from this compartment.

Small molecule inhibitors reveal Niemann-Pick C1 is essential for Ebola virus infection.

Ebola virus entry requires the cholesterol transporter Niemann-Pick C1.

Amino acid substitution in NPC1 that abolishes cholesterol binding reproduces phenotype of complete NPC1 deficiency in mice.

Niemann-Pick type C 1 function requires lumenal domain residues that mediate cholesterol-dependent NPC2 binding.

A novel role for alpha-tocopherol transfer protein (alpha-TTP) in protecting against chloroquine toxicity.

Interaction of AnxA6 with isolated and artificial lipid microdomains; importance of lipid composition and calcium content.

Clues to the mechanism of cholesterol transfer from the structure of NPC1 middle lumenal domain bound to NPC2.

Lysosomal cholesterol activates mTORC1 via an SLC38A9-Niemann-Pick C1 signaling complex.

3.3 Å structure of Niemann-Pick C1 protein reveals insights into the function of the C-terminal luminal domain in cholesterol transport.

Impact of Reduced Cerebellar EAAT Expression on Purkinje Cell Firing Pattern of NPC1-deficient Mice.

Global mapping of Salmonella enterica-host protein-protein interactions during infection.