Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Automatic Gene Ontology annotation based on Rhea mapping
Combined Automated Annotation using Multiple IEA Methods
Molecular cloning and characterization of a novel human beta1,3-glucosyltransferase, which is localized at the endoplasmic reticulum and glucosylates O-linked fucosylglycan on thrombospondin type 1 repeat domain.
B3GALTL transfers glucose to O-fucosyl-proteins
O-glycosylation of TSR domain-containing proteins
Defective B3GALTL does not transfer glucose to O-fucosyl-proteins
Identification and characterization of abeta1,3-glucosyltransferase that synthesizes the Glc-beta1,3-Fuc disaccharide on thrombospondin type 1 repeats.
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B3GLCT recognizes properly folded, O-fucosylated TSR acceptors rather than the tested fucosylated EGF-like domain or unfucosylated modules.
"properly folded TSR-fucose but not fucosylated epidermal growth factor-like
domain"
Mutation analysis of B3GALTL in Peters Plus syndrome.
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All four patients with typical Peters plus syndrome in this eight-patient clinical series had B3GALTL variants; the four overlapping cases had no causative variants detected.
"four of four patients with typical Peters Plus syndrome had mutations in B3GALTL"
Peters plus syndrome mutations disrupt a noncanonical ER quality-control mechanism.
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In the purified TSP1-TSR3 unfolding assay, glucose extension further increased the stability conferred by O-fucose.
"The addition of the glucose further increases the resistance to chemical denaturation."
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The siRNA experiment was interpreted as evidence that B3GLCT is required for ADAMTSL2 secretion.
"significant reduction in secretion of ADAMTSL1, ADAMTSL2, and TSP1(TSR1-3)"
Impaired ADAMTS9 secretion: A potential mechanism for eye defects in Peters Plus Syndrome.
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B3GLCT knockdown reduced secretion of the tested human ADAMTS9-N-L2 fragment; separate mass spectrometry detected the Glc-Fuc glycan on recombinant ADAMTS9 TSRs.
"statistically significant reduction of ADAMTS9 secretion"
O-Fucosylation of ADAMTSL2 is required for secretion and is impacted by geleophysic dysplasia-causing mutations.
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Mouse ADAMTSL2 secretion in HEK293T cells required POFUT2-mediated O-fucosylation, but persisted after B3GLCT knockout.
"B3GLCT was dispensable for proper secretion"
Peters plus syndrome mutations affect the function and stability of human β1,3-glucosyltransferase.
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The human C-terminal D349N substitution abolished glucose-transfer activity, whereas the tested N-terminal E132A substitution retained activity.
"D349N mutant completely lost catalytic activity"
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The 2021 EDTA experiment prompted a suggestion that B3GLCT catalysis might not require a metal ion.
"B3GLCT may not require a metal ion"
Crystal structure of a β1,3-Glucosyltransferase reveals an unusual substrate recognition by a two-domain GT-A fold glycosyltransferase.
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The experimental enzyme-TSR complex shows a substrate-recognition role for the inactive N-terminal GT-A domain beside the active C-terminal domain.
"essential for
substrate binding but is catalytically inactive"