Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Amino-acid substitution in the disordered loop of blood group B-glycosyltransferase enzyme causes weak B phenotype.

Transfusion - 1 Jul 2005

Yazer Mark H, Denomme Greg A, Rose Natisha L, Palcic Monica M

Abstract excerpt

BACKGROUND: Few studies have investigated the reaction kinetics and interactions with nucleotide donor and acceptor substrates of mutant human ABO glycosyltransferases. Previous work identified a B(w) allele featuring a 556G>A polymorphism giving rise to a weak B phenotype. This polymorphism is predicted to cause a M186V amino-acid mutation within a highly conserved series of 16 amino acids present both in both...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to ABO Blood-Group System
Share to Conserved Sequence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Galactosyltransferases

Share to Imaging, Three-Dimensional

Share to N-Acetylgalactosaminyltransferases

Share to Nucleic Acid Amplification Techniques

Share to Protein Structure, Secondary

Share to Substrate Specificity

Source

Identifiers

PMID: 15987364
DOI: 10.1111/j.1537-2995.2005.00170.x

Genes

ABO

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Amino-acid substitution in the disordered loop of blood group B-glycosyltransferase enzyme causes weak B phenotype.PMID 15987364Read ↗

Structural basis for red cell phenotypic changes in newly identified, naturally occurring subgroup mutants of the human blood group B glycosyltransferase.Semantic proximity Read ↗

Aberrant intracellular trafficking of a variant B glycosyltransferase.Semantic proximity Read ↗

Structural basis for the inactivity of human blood group O2 glycosyltransferase.Semantic proximity Read ↗

Identification of a Novel Mutation in B Allele in a Chinese Individual.Semantic proximity Read ↗

Identification of a novel variant c.761C>T on ABO*B.01 gene in ABO glycosyltransferases associated with Bweak phenotype.Semantic proximity Read ↗

Missense mutations outside the catalytic domain of the ABO glycosyltransferase can cause weak blood group A and B phenotypes.Semantic proximity Read ↗

Sequential interchange of four amino acids from blood group B to blood group A glycosyltransferase boosts catalytic activity and progressively modifies substrate recognition in human recombinant enzymes.Semantic proximity Read ↗

An age-dependent ABO discrepancy between mother and baby reveals a novel A(weak) allele.Semantic proximity Read ↗

Evaluation of amino acid substitution p.Asp183Gly of A-glycosyltransferase enzyme in an individual with the AweakB phenotype.Semantic proximity Read ↗

Flexibility and mutagenic resiliency of glycosyltransferases.Semantic proximity Read ↗

Truncated glycosyltransferase coding regions in novel ABO alleles give rise to weak A or B blood group expression and discrepant typing results.Semantic proximity Read ↗

The p.R168Q mutation is associated with the Bw phenotype and a predicted decrease in the stability of the resulting ABO glycosyltransferase.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.