Disease relevance of FUT2

• Recent studies have shown that histo-blood group antigens (HBGAs) and in particular secretor status controlled by the alpha1,2fucosyltransferase FUT2 gene determine susceptibility to norovirus infections, with nonsecretors (FUT2-/-), representing 20% of Europeans, being highly resistant to symptomatic infections with major strains of norovirus [1].
• Modification of cell surface carbohydrates at mucosal surfaces determined by the FUT2 gene may underlie the protective association against heterosexual HIV infection [2].
• Two alpha1,2-fucosyltransferases, expressed in colorectal carcinomas, have been characterized (FUT1 and FUT2 in humans, FTA and FTB in rats) [3].
• Although three antigenically distinct SEC subtypes (SEC1, SEC2, and SEC3) have been reported in the literature, we observed that the isoelectric points of SEC from several Staphylococcus aureus isolates are different from those of any of these three subtypes [4].
• Using the normal gastric mucosa from 60 gastric cancer patients, we assessed immunohistochemically whether type I Le antigen expression depended on the Se and Le genotypes [5].

Psychiatry related information on FUT2

• This study compared the ability of pain readiness to change, as measured by the Pain Stages of Change Questionnaire (PSOCQ), and self-efficacy (SE) ratings, to predict adherence and goal accomplishment in cognitive-behavioral therapy (CBT) for chronic pain [6].
• BACKGROUND: Self-esteem (SE), a widely used construct in the social sciences, is usually conceptualized as a reflection of socialization and interpersonal experiences that may differ considerably between the genders [7].
• CONCLUSIONS: These results are inconsistent with prominent gender-related aetiological models for SE, which postulate that individual differences arise from socialization experiences both within and outside the home of origin which differ widely for the two genders [7].
• A panel analysis revealed support for the indirect effects of physical activity (PA) and self-efficacy (SE) on physical self-worth and global esteem through subdomain levels of esteem [8].
• Decrease in self-esteem (SE) is found in all mood disorders during inter-episode phases [9].

High impact information on FUT2

• We report here the crystal structures of the beta-chain of a TCR complexed with the Staphylococcus aureus enterotoxins C2 and C3 (SEC2, SEC3) [10].
• T cells have been found that bear closely related members of the same V beta family but respond differently to S. aureus toxins; in particular, cells bearing the human V beta 13.2 element respond to toxin SEC2, whereas cells bearing human V beta 13.1 do not [11].
• Recently, the FUT2 and a pseudogene have been isolated, and an Se enzyme-deficient allele (se) caused by a nonsense mutation (G428A, se1) in Caucasians has also been reported [12].
• Although we were unable to find the se1 allele, we have found a missense mutation (A385T, se2) and two nonsense mutations (C571T, se3 and C628T, se4) in the Japanese Se enzyme-deficient alleles [12].
• In addition, we have found a fusion gene, which consisted of the 5'-region of the pseudogene and the 3'-region of the functional FUT2, as a Se enzyme-deficient allele (se5) [12].

Chemical compound and disease context of FUT2

• Thirty-two adult patients, who had been on taurine-free parenteral nutrition for a mean of 59 (SE 14) months for short-bowel syndrome, were studied retrospectively [13].
• After captopril administration, an acceleration threshold value of 440 cm/sec2 for early systolic rise was associated with a sensitivity of 100% and a specificity of 94% for the detection of renal artery stenosis greater than or equal to 50% [14].
• In a second study, a subgroup of ten patients with chronic cholestasis received taurine-enriched (6.0 (SE 0.6) mg/kg per d) parenteral nutrition for 55 (SE 13) months [13].
• Penicillin-sensitive, and gentamicin-sensitive clinical isolates of S. epidermidis (SE) and E. Coli (EC), respectively, were inoculated into freshly drained dialysate of 19 CAPD patients who did not have peritonitis [15].

Biological context of FUT2

• Sequence and expression of a candidate for the human Secretor blood group alpha(1,2)fucosyltransferase gene (FUT2). Homozygosity for an enzyme-inactivating nonsense mutation commonly correlates with the non-secretor phenotype [16].
• We have used the human H blood group alpha(1,2)fucosyltransferase (FUT1) cDNA to screen chromosome 19 cosmid libraries in a search for the human Secretor (Se) blood group gene (FUT2) [17].
• Steady-state FUT2 mRNA levels are cyclically regulated during the estrus cycle, increasing 10-fold from early diestrus to a relative maximum in proestrus [18].
• The methods used in this study are clinically applicable in population studies of the FUT2 gene polymorphism to explore relationships among different ethnic groups and correlations between phenotype and genotype [19].
• Comparative DNA sequence analysis showed the Généthon microsatellite D19S596 lies 2.2 kb downstream of the coding region of FUT1, indicating that the cluster comprising the closely linked FUT1 and FUT2 genes is located 4 cM distal to D19S412 (lod score 13.7) and 9 cM proximal to D19S571 (lod score 11.7) [20].

Anatomical context of FUT2

• FUT2 expression localizes to luminal uterine epithelium by in situ hybridization, implying that this gene determines expression of cell surface Fucalpha1-->2Galbeta epitopes proposed to mediate blastocyst adhesion [18].
• In uterus and colon, a 3.3-kb FUT2 mRNA represents the major fucosyltransferase gene expressed [18].
• The alpha-2-fucosyltransferases: FUT1 (H) of red cells and vascular endothelium and FUT2 (Se) of exocrine secretions [21].
• Molecular basis for erythrocyte Le(a+ b+) and salivary ABH partial-secretor phenotypes: expression of a FUT2 secretor allele with an A-->T mutation at nucleotide 385 correlates with reduced alpha(1,2) fucosyltransferase activity [22].
• COS-7 cells transfected with the SewA385T allele had weak, but detectable, alpha(1,2)fucosyltransferase activity, with an acceptor substrate pattern similar to the wild type FUT2 gene [22].

Associations of FUT2 with chemical compounds

• Molecular analyses of the FUT2 polymorphism of various populations have indicated the ethnic specificity of null alleles: the null allele se(428) is a common Se enzyme-deficient allele in Africans and Caucasians but does not occur in Asians, whereas the null allele se(357,385) is specific to Asians [23].
• When 39 SEC S. aureus strains isolated from fecal samples of randomly selected diarrheal patients associated with food-borne outbreaks in central Taiwan in 6 years (1995-2000) were analyzed, it was found that the major SEC subtypes for these S. aureus strains were SEC2 and C3 [24].
• The H enzyme has a much lower Km for phenyl-beta-galactoside than does the Se enzyme [25].
• The 299-bp Se, 146-bp sej and/or 312-bp se(fus) allele-specific products were amplified and detected in the native polyacrylamide gel [26].
• Northern blot analysis in wild-type mice shows 15-fold elevations of Fut2 steady-state mRNA with estradiol treatment, whereas Fut1 varies little [27].

Regulatory relationships of FUT2

• All Le(a+b-) individuals (nonsecretors) were homozygous for the FUT2 G428A mutation and all Le(a-b-) individuals had inactivating mutations on both FUT3 alleles [28].

Other interactions of FUT2

• Sec1 and Sec2 are separated by 12 kb and are 65.5 kb and 35 kb apart, respectively, from the FUT1 gene [17].
• The Lewis (Le) histo-blood group system comprises two major antigens, Le(a) and Le(b) which are determined by alpha (1,2)-fucosyltransferase (FUT2) and alpha (1,3/1,4)-fucosyltransferase (FUT3) [29].
• The human secretor type alpha(1,2)fucosyltransferase gene (FUT2) polymorphism was investigated in Xhosa and Caucasian populations of South Africa by polymerase chain reaction-restriction fragment length polymorphism and DNA sequencing [30].
• However, it appears that APOC2 may be closely linked to the blood group loci Lutheran (Lu) and Secretor (Se), and probably less closely linked to Lewis (Le) [31].
• F(ST) between the Asians and the others measured at FUT2 was higher than at FUT6 [32].

Analytical, diagnostic and therapeutic context of FUT2

• A PCR method using sequence-specific primers for FUT2 genotyping in whites was developed [33].
• In addition, we did not detect any hybridized band corresponding to the FUT2 by Southern blot analysis using the catalytic domain of the FUT2 as a probe, indicating that the three individuals were homozygous for a gene deletion in the FUT2 [34].
• Sequence analysis of the cosmids resulted in the characterization of an open reading frame (ORF), 1098 bp in length, that is 82.3% identical to the human FUT1 sequence; a second ORF, 1023 bp in length, 85% identical to the human FUT2 sequence; and a third FUT-like sequence thought to be a pseudogene [35].
• STUDY DESIGN AND METHODS: The applicability of denaturing high-performance liquid chromatography (DHPLC) analysis was evaluated for genotyping the FUT2 in two Sri Lankan populations (Tamil and Sinhalese) [36].
• Molecular cloning and characterization of the pig secretor type alpha 1,2fucosyltransferase (FUT2) [37].

References