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BRENDA support

Literature summary for 3.1.3.9 extracted from

  • Hayee, B.; Antonopoulos, A.; Murphy, E.J.; Rahman, F.Z.; Sewell, G.; Smith, B.N.; McCartney, S.; Furman, M.; Hall, G.; Bloom, S.L.; Haslam, S.M.; Morris, H.R.; Boztug, K.; Klein, C.; Winchester, B.; Pick, E.; Linch, D.C.; Gale, R.E.; Smith, A.M.; Dell, A.; Segal, A.W.
    G6PC3 mutations are associated with a major defect of glycosylation: a novel mechanism for neutrophil dysfunction (2011), Glycobiology, 21, 914-924.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Source Tissue

Source Tissue Comment Organism Textmining
blood
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Homo sapiens
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General Information

General Information Comment Organism
malfunction G6PC3 mutation induces major alterations in neutrophil N- and O-glycomes Homo sapiens