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The Le(a) and Le(b) human blood group antigens are synthesized in tissues producing exocrine secretions; they also circulate in plasma, where they are adsorbed by erythrocytes. They are synthesized by two fucosyltransferases, encoded by Lewis (FUT3) and secretor (FUT2) loci. This genetic model has been challenged because some erythrocyte Lewis-negative(More)
Six human alpha-L-fucosyltransferase genes have been registered in the GDB as FUT1 to FUT6 according to the chronology of their description. FUT1 and FUT2 encode the alpha(1,2)fucosyltransferases H and Se respectively. The FUT2 gene has not been cloned, but it is expected to be closely linked to FUT1 on the long arm of chromosome 19. FUT3, FUT4, FUT5 and(More)
While most humans express an alpha(1,3)-fucosyltransferase in plasma, 9% of individuals on the isle of Java (Indonesia) do not express this enzyme. Ninety-five percent of these plasma alpha(1,3)-fucosyltransferase-deficient individuals have Lewis negative phenotype on red cells, suggesting strong linkage disequilibrium between these two traits. To define(More)
The last step in the biosynthesis of Le(x) antigen, the addition of a fucose to precursor polysaccharides, can be catalyzed by different alpha-3-fucosyltransferases. We localized the gene (FUT4) encoding myeloid alpha-3-fucosyltransferase by PCR assay using panels of somatic cell and radiation hybrids which retain different rearrangements of chromosome 11.(More)
Using a panel of 25 somatic cell hybrids, we have regionally localized 112 microsatellite markers generated by Généthon and assigned to chromosome 11. A genetic map of 74 of them was produced using linkage analysis of the eight largest CEPH (Centre d'Etude du Polymorphisme Humain) families. They could be ordered on chromosome 11 with an average distance of(More)
In order to better characterize the chromosomic rearrangement of an unbalanced 45XX t(X;22) (q28;q11) DiGeorge patient, a somatic hybrid clone segregating the translocated chromosome was constructed and investigated using X and 22 linked markers. Our study demonstrated that this de novo translocation was from paternal origin. The breakpoint was assigned(More)
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