ArticleScientific reports2023
FUT1 variants responsible for Bombay or para-Bombay phenotypes in a database.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- A novel FUT1 variant, c.[35C>T;133_136dupCGCC], underlies a group A para-Bombay phenotype in a Chinese blood donor.Vox sanguinis · 2026Article
- Identification and structural analysis of a novel FUT1 c.789C>A variant and previously reported para-Bombay alleles using an α2FucT1 structural model.Transfusion · 2026Article
- Review
- Mutations Inactivating Biosynthesis of Dispensable Carbohydrate-Antigens Prevented Extinctions in Primate/Human Lineage Evolution.Journal of molecular evolution · 2025Review
- Exploring the diverse biological significance and roles of fucosylated oligosaccharides.Frontiers in molecular biosciences · 2024Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rare individuals with Bombay and para-Bombay phenotypes lack or have weak expression of the ABO(H) antigens on surface of red blood cells due to no or very weak H-type α(1,2)fucosyltransferase activity encoded by FUT1. These phenotypes are clinically important because subjects with these phenotypes can only accept transfusions of autologous blood or blood from subjects with the same phenotypes due to the anti-H antibody. To survey FUT1 alleles involved in Bombay and para-Bombay phenotypes, the effect of 22 uncharacterized nonsynonymous SNPs in the Erythrogene database on the α(1,2)fucosyltransferase activity were examined by transient expression studies and in silico analysis using four different online software tools. Two nonfunctional alleles (FUT1 with c.503C>G and c.749G>C) and one weakly functional allele (with c.799T>C) were identified in transient expression studies, while the software predicted that the proteins encoded by more alleles including these would be impaired. Because both nonfunctional FUT1 alleles appear to link to the nonsecretor alleles, homozygotes of these alleles would be of the Bombay phenotype. The present results suggest that functional assays are useful for characterization of nonsynonymous SNPs of FUT1 when their phenotypes are not available.
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