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#blood group antigens

2 public questions tagged with this topic.

Which of the following plays a role in blood group antigen formation?

Glycosylation modifications influence ABO antigen presentation beyond core transferase reactions involving fucose GalNAc Gal additions to H substance. Sialic acid N acetylneuraminic acid added ST3GAL ST6GAL1 sialyltransferases using CMP Neu5Ac caps galactose residues precursor polylactosamine chains via alpha two three alpha two six linkages introducing negative charge repelling pathogens masking H antigen lectin binding modulating accessibility and complement regulation. On erythrocyte membrane glycophorin A carries fifteen O linked one N linked sialylated tetrasaccharides accounting major negative zeta potential minus fifteen millivolts reducing aggregation controlling alternative complement via factor H binding sialic acid polyanion host marker. ABO antigens reside same polylactosamine carriers sialylation status regulates accessibility terminal GalNAc Gal anti A anti B IgM agglutination and lectin Dolichos biflorus DBA. Sialic acid also serves receptor influenza hemagglutinin Plasmodium EBA175 invasion. Phosphatidylinositol triacylglycerol ergosterol do not contribute extracellular glycan epitopes blood group serology. Thus sialic acid role modulator antigen formation red cell surface properties exemplifies glycobiology intersection transfusion science infectious disease susceptibility immune evasion mechanisms tested serology exams and immunohematology contexts and ABO discrepancies.

Ref: Varki A., Glycobiology 2008, Sialic acids blood group antigen modulation masking and recognition.

Which of the following enzymes is NOT involved in blood group antigen synthesis?

Blood group oligosaccharide construction depends nucleotide sugar utilizing glycosyltransferases retaining mechanism not phosphoinositide hydrolyzing enzymes that cleave glycerophosphate bonds. Formation H requires GDP fucose dependent FUT1 FUT2 FUT2 secretor adding fucose alpha one two linkage Gal. Conversion A uses UDP GalNAc dependent alpha one three N acetylgalactosaminyltransferase GTA adding GalNAc, B uses UDP Gal dependent galactosyltransferase GTB adding galactose both GT6 family retaining via SNi like mechanism. These catalyze glycosidic bond formation with retention stereochemistry requiring manganese. Phospholipase C isozymes PLC beta gamma delta epsilon hydrolyze phosphatidylinositol four five bisphosphate at glycerophosphate bond generating diacylglycerol activating PKC RasGRP and inositol trisphosphate releasing calcium via IP3 receptors ER. Its active site X Y domains bind calcium C2 domain distinct GT fold Rossmann. Thus PLC participates calcium signaling downstream GPCR RTK not glycan anabolism. Confusing PLC glycosyltransferases mixes two lipid pathways. Understanding enzymatic classification helps predict inhibition U73122 for PLC versus substrate analogs for blood group enzymes separating immunogenetics second messenger biology important biochemistry exams distinguishing transferase versus hydrolase reactions and metabolic contexts and physiological roles.

Ref: Patenaude et al., Transfusion 2002, ABO synthetic enzymes versus phospholipase C role distinction.