anti-Fucosyltransferase 7 (Alpha (1,3) Fucosyltransferase) (FUT7) Antibodies

Cow (Bovine) Fucosyltransferase 7 (Alpha (1,3) Fucosyltransferase) (FUT7) interaction partners

1. The bfut7 gene encodes an enzyme that mainly ensures the synthesis of the sialyl-lewis X motif.

Human Fucosyltransferase 7 (Alpha (1,3) Fucosyltransferase) (FUT7) interaction partners

1. Knockdown of FUT7 inhibits human hepatocarcinoma cell proliferation.

2. FUT7 silencing causes inhibition of adhesion and migration of HepG2 hepatocellular carcinoma cells in vitro.

3. FUT7 overexpression significantly promoted monocyte-endothelial adhesion, while FUT7 knockdown obviously inhibited IL-1beta-induced monocyte-endothelial adhesion

4. The DNA demethylation within the fut7 gene controls selectin ligand expression in humans, including the inducible topographic commitment of T cells for skin and inflamed sites.

5. This study presents the first example of a distinct regulatory mechanism involving transcriptional down-regulation of Fut7 by MAPCs that could modulate the trafficking behavior of T cells in vivo.

6. After transfection of JAR cells with fucosyltransferase VII, the expression of FUT7 and sLeX synthesis were increased, and the percent adhesion of trophoblast cells to RL95-2 cell monolayer was significantly increased.

7. Overexpression of alpha1,3 FucT-VII promoted the expression of CD24 and SLe X and is associated with colorectal carcinoma metastases.

8. The Fuc-T VII promoter is transactivated by Tax in concert with CBP through a CRE-like sequence in a manner similar to that of viral CRE in HTLV-1 LTR.

9. H-Ras mediates FucT-VII induction in Jurkat T cells via the activation of the Raf, PI3K, and a distinct, H-Ras-specific effector signaling pathway.

10. These results suggest that the FucT-VII may be a major regulator of the biosynthesis of the sLe(x)-epitopes on T lymphoblasts.

11. human FucT-IV and -VII both contribute and cooperate in regulating L-selectin-, P-selectin-, and E-selectin-dependent rolling on PSGL-1, with FucT-VII playing a predominant role in conferring selectin binding activity to PSGL-1

12. A differential functional impact of N-glycosylation on C2GnT-1 and FucT-VII and disclose that a strongly reduced FucT-VII activity retains the ability to fucosylate PSGL-1 on the core2-based binding site(s) for the three selectins.

13. Alpha 1,3-fucosyltransferase-VII regulates the signaling molecules of the insulin receptor pathway

14. The up regulation of alpha1,3FucT-VII mRNA and cell surface SLe(x) (alpha1,3FucT-VII product) by UV and down regulation of them by ATRA was speculated to be one of the mechanisms that alpha1,3FucT-VII decreased and increased [susceptibility to] apoptosis.

15. Overexpression of fucosyltransferase VII (FUT7) promotes embryo adhesion and implantation.

16. This is the first time to report that alpha1,3FucT-VII can regulate the mRNA expression of integrin.

Mouse (Murine) Fucosyltransferase 7 (Alpha (1,3) Fucosyltransferase) (FUT7) interaction partners

1. The DNA demethylation within the fut7 gene controls selectin ligand expression in mice, including the inducible topographic commitment of T cells for skin and inflamed sites.

2. Cloning of an intragenic region spanning a 1kb region upstream of exon 4 into an enhancer-containing vector indeed elicited fut7 promoter activity in cd4 positive T cells.

3. These results demonstrate that all genetic information essential for appropriate and selective expression of Fut7 in diverse cell types and in response to distinct developmental signals is contained within this comparatively small genetic region.

4. alpha(1,3)-Fucosyltransferases FUT4 and FUT7 control murine susceptibility to thrombosis.

5. Functional PSGL-1 generated by basophil FT-IV/VII and its subsequent binding to L-selectin could be one of the essential steps required for initial basophil recruitment and the development of IgE-chronic allergic inflammation in mice.

6. striking differences between the requirement of FucT-VII and C2GlcNAcT-I for Ligands for E-selectin and P-selectin expression in CD4+ T cells.

7. Loss of the barrier protective molecule TFF3 leads to a profound increase in susceptibility to DSS-induced colitis, and this can be abrogated by reducing Fuc-TVII-dependent leukocyte recruitment.

8. FucT-VII is an important pathophysiologic mediator of renal ischemia reperfusion injury, structural damage, and neutrophil infiltration postischemia.

9. Efficient recruitment of activated lymphocytes to the brain in a model mimicking early inflammation during experimental allergic encephalomyelitis is controlled by FucT-VII.

10. FT-IV and FT-VII are both important contributors to selectin-dependent eosinophil recruitment to the skin and may represent therapeutic targets for treating diseases in which eosinophil recruitment contributes to pathophysiology.

11. Keratan sulfate sulfotransferase competes with FucT-VII for the same acceptor substrate and downregulates the synthesis of L-selectin ligand by inhibiting alpha1,3-fucosylation.

12. a deficiency in Fuc-TVII, and in a more pronounced fashion, a combined deficiency in both Fuc-TIV and Fuc-TVII, leads to accelerated death following M. tuberculosis infection