EC Number   |
General Information |
Reference |
|---|
   2.4.1.152 | malfunction |
suppression of isoform Fut10 expression induces the differentiation of neural stem cells and embryonic stem cells. In addition, knockdown of Fut10 expression in the cortical ventricular zone of the embryonic brain impairs the radial migration of neural precursor cells |
736427 |
| 2.4.1.152 | metabolism |
the enzyme is specifically responsible for Sialyl-Lewis X synthesis |
721939 |
| 2.4.1.152 | physiological function |
following FUT7 siRNA transfection, the expression of FUT7 is markedly downregulated. The synthesis of sialyl-Lewisx epitope is also inhibited, consistent with the downregulated expression of FUT7. MHCC-97 cell proliferation is also significantly inhibited following FUT7 siRNA transfection, which is correlated with suppression of the S-phase in cell cycle progression. The knockdown of FUT7 inhibits the activation of phospholipase Cgamma by inhibiting its translocation and phosphorylation |
756981 |
| 2.4.1.152 | physiological function |
fucosyltransferase IV is implicated in the modulation of cell migration, invasion and cancer metastasis. The enzyme has a role in epithelial-mesenchymal transition through activation of the phosphatidylinositol 3-kinase/Akt and nuclear factor-kappaB signaling systems, which induce the key mediators Snail and MMP-9 and facilitate the acquisition of a mesenchymal phenotype |
735901 |
| 2.4.1.152 | physiological function |
FUT7 overexpression significantly promotes monocyte-endothelial adhesion, while FUT7 knockdown inhibits IL-1beta-induced monocyte-endothelial adhesion. Fucosylation of selectin ligand endomucin is directly involved in IL-1beta-induced monocyte-endothelial adhesion. p38 and extracellular signal-regulated kinase (ERK) MAPK signaling pathway are activated by IL-1beta, while inhibition of the p38/ERK signaling pathway decreases FUT7 expression level and IL-1beta-induced monocyte-endothelial adhesion |
757537 |
| 2.4.1.152 | physiological function |
glycoproteins from tobacco line xFxG1, in which expression of a hybrid beta-(1-4)-galactosyltransferase and a hybrid a-(1-3)-fucosyltransferase IXa (FUT9a) is combined, contain an abundance of hybrid N-glycans with Lewis X (LeX) epitopes |
703055 |
| 2.4.1.152 | physiological function |
knocking-out of two XylT genes and four FucT genes in BY-2 suspension cells using CRISPR/Cas9. Three lines show a strong reduction of beta(1,2)-xylose and alpha(1,3)-fucose, while two lines are completely devoid of them, indicating complete gene inactivation. The KO lines do not show any particular morphology and grow as the wild-type. A KO line transformed with genes encoding a human IgG2 antibody shows an IgG2 expression level as high as in a control transformant. The IgG glycosylation profile shows no beta(1,2)-xylose or alpha(1,3)-fucose present on the glycosylation moiety. The dominant glycoform is the GnGn structure |
756828 |
| 2.4.1.152 | physiological function |
largest amount of recombinant FucT-IX is obtained in Sf9-insect cells by use of a baculovirus inducible protein production system |
703540 |
| 2.4.1.152 | physiological function |
overexpression of FUT6 in hepatocellular carcinoma cells enhance S-phase cell population, promoted cell growth and colony formation ability. FUT6 plays an important role in hepatocellular carcinoma cell growth by regulating the phosphatidyl inositol 3-kinase/Akt signaling pathway |
721501 |
| 2.4.1.152 | physiological function |
overexpression of isoform Fut10 enhances the self-renewal of neural stem cells |
736427 |
