anti-Fucosyltransferase 1 (Galactoside 2-alpha-L-Fucosyltransferase, H Blood Group) (FUT1) Anticorps

Mouse (Murine) Fucosyltransferase 1 (Galactoside 2-alpha-L-Fucosyltransferase, H Blood Group) (FUT1) interaction partners

1. miR-339-5p downregulation contributes to Taxol resistance in small-cell lung cancer by targeting FUT1.

2. Fut1 plays an important role in regulating angiogenesis and ICAM-1 expression in inflammatory arthritis.

3. We found that Fut1 mRNA and Fut4 mRNA were upregulated, while Fut2 mRNA and Fut9 mRNA were downregulated by androgen in the caput epididymis.

4. fucosyltransferase (Fut)-deficient (Fut1, Fut2 and Fut4) mice which lack LeX or LeY antigen are still fertile.

5. These results indicate that Fut2-mediated fucosylated epithelial cells (F-ECs) share M cell-related fucosylated molecules but maintain distinctive EC characteristics, Fut1 is, therefore, a reliable marker for M cells.

6. FUT1 is essential for fucosylation of glycolipid GA1 in the pancreas.

7. In null mutant mice lacking FUT1, the absence of blood group H carbohydrate resulted in the delayed maturation of the glomerular layer of the main olfactory bulb.

8. Vasculogenesis was the most clearly affected by FUT1 expression, suggesting that tumor angiomorphogenesis may depend on E-selectin-mediated interaction between HCC and endothelial cells, the inhibition of which remarkably retards tumor growth.

Human Fucosyltransferase 1 (Galactoside 2-alpha-L-Fucosyltransferase, H Blood Group) (FUT1) interaction partners

1. In patients with hepatocellular carcinoma, Kaplan Meier survival analysis showed significantly shorter relapse-free survival for those with high expression of FUT1.

2. FUT1 promotes Taxol resistance of ovarian carcinoma through apoptosis-related proteins

3. The expression of FUT1, an alpha-1,2 fucosyltransferase, is remarkably down-regulated during melanoma progression, and the ectopic expression of FUT1 is sufficient to inhibit invadopodium formation and ECM degradation.

4. FUT1 mutations responsible for the H-deficient phenotype in the Polish population, including the first example of an abolished start codon.

5. The overexpression of miR-140-5p/149 inhibited apoptosis and promoted proliferation and autophagy of human primary chondrocytes via downregulating FUT1.

6. Results show that c-Fos binding to TPA response element of FUT1 promoter enhances the activation of FUT1 transcription by c-Jun.

7. miR-339-5p downregulation contributes to Taxol resistance in small-cell lung cancer by targeting FUT1.

8. High FUT1 expression is associated with breast cancer.

9. downregulation of FUT1, which leads to the perinuclear localization of LAMP-1 and 2, is correlated with increased rate of autophagic flux by decreasing mTOR signaling and increasing autolysosome formation.

10. The H blood group system is defined by a terminal fucose residue found on red blood cells and in secretions formed by the action of alpha-1,2-fucosyltransferases 1 (alpha2FucT1) and 2 (alpha2FucT2), respectively. Mutant alleles of the corresponding FUT1 and FUT2 genes result in either a H- phenotype (Bombay phenotype) or a weak H phenotype (para-Bombay). Review.

11. Two novel FUT1 mutations have been identified in the proband's FUT1 gene. The insertion mutation in the FUT1 that caused a shift of the open reading frame and formed a termination codon early at Amino Acid Position 334 may be the main reason for H deficiency in this case.

12. Protein O-fucosyltransferase 1 promotes trophoblast cell proliferation by activating MAPK and PI3K/Akt signaling pathways.[poFUT1]

13. Data suggest that the identification of genes in response to alpha1,2-fucosyl transferase (FUT1) may provide a theoretical basis for the investigations of the molecular mechanism of ovarian cancer.

14. alpha(1,2)-fucosyltransferase activity is involved in the development of multidrug resistance of chronic myeloid leukemia cells probably through FUT1 regulated the activity of EGFR/MAPK signaling pathway and the expression of P-gp.

15. data confirm the hypothesis that the h2 allele is linked to Se(357, 716), and the concurrence of unique FUT1 and FUT2 mutations is geographically specific.

16. We show that fut1 in RA synovial fibroblasts is important in angiogenesis, leukocyte-synovial fibroblast adhesion, and synovial fibroblast proliferation

17. Fut1 plays an important role in regulating angiogenesis and ICAM-1 expression in inflammatory arthritis.

18. FUT1 mediates c-Jun-induced cell proliferation in ovarian cancer cells.c-Jun transcriptionally modulates FUT1 expression in ovarian cancer cells.

19. Data indicate that single nucleotide polymorphism (SNPS) in the 3'-untranslated region of the fucosyltransferase 1 (FUT1) gene and intron of the syntaxin 1B (STX1B) gene were the top hits for Kawasaki disease (KD) susceptibility.

20. Data indicate that alpha -1,2 fucosyltransferase (FUT1) 682A> G and 547_552delAG mutations do not affect the transcript efficiency, although various mutations have different impact on the enzyme's activity.

Pig (Porcine) Fucosyltransferase 1 (Galactoside 2-alpha-L-Fucosyltransferase, H Blood Group) (FUT1) interaction partners

1. Results highlight the role of MUC4 and FUT1 on pig intestinal homoeostasis and improved the knowledge regarding the potential interaction between host genetics, gut microbiota composition and host metabolism in a healthy status.

2. FUT1 expression levels and low FUT2 expression levels in the intestines of Sutai pigs affected FUT1 and FUT2 enzymes, the synthesis of type 2 H and type 1 H antigens, and E. coli F18 adhesion. Moreover, low FUT2 expression levels conferred resistance to E. coli F18.

3. Polymorphism of FUT1 and MUC4 associated with resistance to colibacteriosis was determined.

4. The 5'-flanking region of the FUT1 gene (-1150 to +50 bp) exhibited promoter activity and the -1150-bp to -849-bp region showed negative regulation of the gene.

5. Studied the beneficial effects of alpha (1,2)-fucosyltransferase (FUT1) M307 (A) on piglet survival on commercial farms. Piglet survival for individuals with the AA genotype was almost two-fold greater than for GG individuals.

6. The results indicated that Sutai pigs with the AA genotype in M307 of FUT1 gene have relatively strong general disease resistance ability in piglets.

7. The mutation at M307 in the FUT1 gene determines susceptibility of small intestinal epithelium to E. coli F18 adhesion in Sutai piglets.

8. FUT1 mutations might play a role in pig infection by multi-pathogens, and the AA may be a favourable genotype for increasing the resistance to disease.

9. Beneficial genotype of swine FUT1 gene governing resistance to E. coli F18 is associated with important economic traits

10. transgenic male pigs were produced that possess an alpha alpha-1,3-galactosyltransferase knockout allele and express a randomly inserted human alpha 1,2-fucosylosyltransferase transgene

11. Genetic variability is assocated with reproductive traits.

12. Results showed that the genetic polymorphisms of the FUT1 locus were only detected in the 3 exotic pig breeds and indicated that FUT 1 gene and the type of breeds significantly affected total number born.

13. Results indicated that Chinese native pig breeds lack the genetic background, FUT1 genetic polymorphisms, on the resistance to ETEC F18 bacteria.

14. results showed that genetic polymorphisms of the FUT1 locus were only detected in western pig breeds & the Chinese Taihu, Huai & Lingao breeds; results indicated that Chinese native pig breeds lack genetic factors providing resistance to ETEC F18 bacteria

Cow (Bovine) Fucosyltransferase 1 (Galactoside 2-alpha-L-Fucosyltransferase, H Blood Group) (FUT1) interaction partners

1. Data show that si-RNA induced down-regulation of FUT1 and FUT2 reduced expression of fucosylated nucleolin glycoforms and their exposure at the cell surface.