EC Number   |
Expression |
Reference |
|---|
   2.4.1.152 | down |
FUT4 staining is weak in proliferative and menstrual endometrium. Inductive effect of progesterone on FUT4 transcription is lost after 48 h of treatment |
706697 |
| 2.4.1.152 | down |
protein kinase R inhibitors 2-aminopurine and C16 inhibit FUT3, FUT5, and FUT6 expression. MG-132 inhibits the IMD-0354-dependent transcription of FUT5 in a dose-dependent manner |
703902 |
| 2.4.1.152 | more |
the mRNA and protein expression levels of FUT7 are high in the MHCC-97 cell line compared with levels in normal liver cells |
756981 |
| 2.4.1.152 | up |
breast cancer cell lines display increased expression of isoform FUT4 |
735901 |
| 2.4.1.152 | up |
FUT4 mRNA is significantly upregulated during the early and midsecretory stages of the menstrual cycle compared with the other menstrual phases, with maximal expression during the mid-secretory phase. In proliferative explants, progesterone significantly increases FUT4 transcription and translation after 24 h in culture. Estrogen does not have any significant effects |
706697 |
| 2.4.1.152 | up |
higher mRNA and protein expression of the enzyme are observed in colorectal tumors compared with adjacent normal ones |
723313 |
| 2.4.1.152 | up |
in hepatocellular carcinoma tissues, the expression levels and activity of alpha1,3/4-fucosyltransferase FUT6 are significantly up-regulated |
721501 |
| 2.4.1.152 | up |
protein kinase R function is essential for FUT3, FUT5, and FUT6 induction and sLex expression in Herpes simplex virus type 1-infected cells. IMD-0354, an inhibitor of the NF-kappaB-activating factor IKK-2, induces FUT transcription via a IKK-2-independent mechanism, irrespective of whether the cells are virus-infected or not |
703902 |
| 2.4.1.152 | up |
treatment with inflammatory factors interleukin-1beta pronouncedly upregulates alpha1,3-fucosyltransferase VII gene (FUT7) mRNA and protein expression level in EA.hy926 endothelial cells |
757537 |
| 2.4.1.152 | up |
two hepatocyte nuclear factor-4alpha (HNF-4alpha) and one octamer binding transcription factor-1 (Oct-1) binding sites are essential for FUT VI transcription, which are the 5'-flanking regions at positions -156 to -136 nt and -56 to -19 nt relative to the FUT VI gene transcription start site. Transient overexpression of HNF-4alpha but not Oct-1 enhances both FUT VI promoter activities and FUT VI mRNA levels in HuH-7 cells. FUT VI mRNA levels are higher in HepG2 cells than in HNF-4alpha-transfected HuH-7 cells |
704786 |
