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
Combined Automated Annotation using Multiple IEA Methods
Genomic structure, mapping, and expression analysis of the mammalian Lunatic, Manic, and Radical fringe genes.
Fringe is a glycosyltransferase that modifies Notch.
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Fringe proteins are O-fucose-specific beta1,3-GlcNAc-transferases acting on Notch EGF repeats.
"Drosophila and mammalian Fringe proteins possess a fucose-specific beta1,3 N-acetylglucosaminyltransferase activity that initiates elongation of O-linked fucose residues attached to epidermal growth factor-like sequence repeats of Notch."
Mutation of the fucose-specific beta1,3 N-acetylglucosaminyltransferase LFNG results in abnormal formation of the spine.
Proteomic analysis of cerebrospinal fluid extracellular vesicles: a comprehensive dataset.
Defective LFNG does not transfer GlcNAc to Pre-NOTCH
Falcon deep research report on human LFNG
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LFNG enhances DLL1- and inhibits JAG1-induced signaling (galactose-dependent).
"Addition of galactose to the Fringe-added GlcNAc by β1,4-galactosyltransferases (B4GALT1) **enhances LFNG's positive effect on DLL1-induced Notch signaling** but is required for LFNG-mediated inhibition of JAG1 signaling"
UniProtKB entry Q8NES3 (LFNG_HUMAN)
Manic fringe and lunatic fringe modify different sites of the Notch2 extracellular region, resulting in different signaling modulation.
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LFNG reduces JAG1- but not DLL1-triggered NOTCH2 signaling.
"We also found that both fringe proteins reduced Jagged1-triggered Notch2 signaling, whereas neither affected Delta1-triggered Notch2 signaling."
Identification of novel LFNG mutations in spondylocostal dysostosis.
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SCDO3 LFNG DxD missense variant abolishes enzyme activity.
"The missense variant was in the DxD motif, an active-site motif of the glycosyltransferase, and its loss of the enzyme function was confirmed by an in vitro enzyme assay."
Modulation of notch-ligand binding by protein O-fucosyltransferase 1 and fringe.