EC Number   |
General Information |
Reference |
|---|
   2.4.1.221 | evolution |
CePOFUT1 is a member of the GT65 family and contains four conserved disulfide bridges through the GT65 family |
723541 |
| 2.4.1.221 | evolution |
POFUT2 belongs to the classical GT-B fold family of glycosyltransferases with two closely interacting Rossmann-like domains. POFUT2 shows a variation of the classical GT-B fold |
722118 |
| 2.4.1.221 | evolution |
the highly correlated presence of POFUT1 and fucosylatable hEGFs has accompanied animal evolution |
759817 |
| 2.4.1.221 | malfunction |
cell proliferation of POFUT1 knockdown cells is significantly inhibited compared with that of control cells, phenotypes, overview |
736272 |
| 2.4.1.221 | malfunction |
CHO cells lacking Pofut1 express Notch receptors on the cell surface at similar levels to wild-type cells |
703986 |
| 2.4.1.221 | malfunction |
CRISPR-mediated knockout of POFUT1 in U2OS cells suppresses both normal Notch1 signaling, and the ligand-independent signaling associated with leukemogenic mutations of Notch1. Normal and oncogenic signaling are rescued by wild-type POFUT1 but rescue is impaired by an active-site R240A mutation |
759308 |
| 2.4.1.221 | malfunction |
deletion of Pofut1 leads to global defects in Notch signaling and death of mice at E9.5, with a phenotype consistent with inactivation of signaling by the four Notch receptors. Embryonic stem cells lacking Pofut1 express Notch receptors on the cell surface at similar levels to wild-type cells. In mouse somites, there is evidence of altered Notch trafficking in the absence of Pofut1, consistent with reduced cell surface expression |
703986 |
| 2.4.1.221 | malfunction |
elimination of Pofut1 in mice causes embryonic lethality with Notch-like phenotypes, elimination of Pofut2 results in an early embryonic lethal phenotype in mice |
722369 |
| 2.4.1.221 | malfunction |
elimination of Pofut1 in mice has a profound effect on ligand binding in both embryonic stem cells and lymphoid cells. A small decrease in cell surface expression of Notch proteins is seen in embryonic stem cells lacking Pofut1 and in somites from mice with a hypomorphic allele of Pofut1, cax |
722090 |
| 2.4.1.221 | malfunction |
embryonic stem cells lacking Pofut1 are deficient in Notch ligand binding, have wild-type levels of cell surface Notch receptors. Pofut1-/- embryonic stem cells do not bind Notch ligands or exhibit Notch signaling. Overexpression of fucosyltransferase-defective Pofut1 R245A in Pofut1-/- cells partially rescues ligand binding and Notch signaling, but this effect is not specific. Under certain conditions, mammalian Notch receptors can bind Notch ligands and transduce a Notch signal in the absence of Pofut1 and O-fucose |
704420 |
