• Publications
  • Influence
Divergent evolution of fucosyltransferase genes from vertebrates, invertebrates, and bacteria.
TLDR
A model for the evolution offucosyltransferase genes by successive duplications, followed by divergent evolution is proposed, with either two different ancestors for the alpha-2/6-fucosytransferases and one for thealpha-3-fukosyl transferases or a single common ancestor for the two families.
The animal sialyltransferases and sialyltransferase-related genes: a phylogenetic approach.
The animal sialyltransferases are Golgi type II transmembrane glycosyltransferases. Twenty distinct sialyltransferases have been identified in both human and murine genomes. These enzymes catalyze
Genetics of ABO, H, Lewis, X and Related Antigens
TLDR
The phylogeny of ABH determinants shows that they appeared as tissular antigens much earlier than as red cellAntigens, and an effort is made to correlate their tissular distribution in the adult with the embryological origin of each tissue.
Common origin and evolution of glycosyltransferases using Dol-P-monosaccharides as donor substrate.
TLDR
It is proposed that the endoplasmic reticulum glycosyltransferases using Dol-P-monosaccharides as donor substrate have a multispan transmembrane topology with a first large luminal conserved loop containing the long motif and a small cytosolic conservedloop containing the short motif, different from the classical type II glycosYLtransferases, which are anchored in the Golgi by a single transmemBRane domain.
A new superfamily of protein-O-fucosyltransferases, α2-fucosyltransferases, and α6-fucosyltransferases: phylogeny and identification of conserved peptide motifs
TLDR
Evidence that the present genes encoding for these enzymes have originated from a common ancestor by duplication and divergent evolution, suggests that they constitute a new superfamily of fucosyltransferases.
Activity, Splice Variants, Conserved Peptide Motifs, and Phylogeny of Two New α1,3-Fucosyltransferase Families (FUT10 and FUT11)*
We report the cloning of three splice variants of the FUT10 gene, encoding for active α-l-fucosyltransferase-isoforms of 391, 419, and 479 amino acids, and two splice variants of the FUT11 gene,
Molecular basis for Lewis alpha(1,3/1,4)-fucosyltransferase gene deficiency (FUT3) found in Lewis-negative Indonesian pedigrees.
TLDR
This work sequenced FUT3 in Lewis-negative individuals and identified two single base pair changes that can account for erythrocyte/saliva-discrepant Lewis typing results.
Molecular genetics of H.
TLDR
Most inactivating mutations of FUT1 and FUT2 genes are located in the coding region of the genes and are nonprevalent sporadic mutations of relative recent appearance.
Genetic complementation reveals a novel human congenital disorder of glycosylation of type II, due to inactivation of the Golgi CMP-sialic acid transporter.
TLDR
It is concluded that this defect is a new type of congenital disorder of glycosylation (CDG) of type IIf affecting the transport of CMP-sialic acid into the Golgi apparatus.
FUT4 and FUT9 genes are expressed early in human embryogenesis.
TLDR
The tissue expression of the embryonic FUT9 transcript is closer to that observed for the mouse (brain), than to the known human (stomach) transcripts, and the acceptor specificity and the kinetics of the alpha3-fucosyltransferase encoded by this FUT 9 transcript are similar to the FUT4 enzyme, except for the utilization of the lac-di-NAc acceptor which is not efficiently transformed by the F UT9 enzyme.
...
...