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Targeted disruption of Gb3/CD77 synthase gene resulted in the complete deletion of globo-series glycosphingolipids and loss of sensitivity to verotoxins.

To examine whether globotriaosylceramide (Gb3/CD77) is a receptor for verotoxins (VTs) in vivo, sensitivity of Gb3/CD77 synthase null mutant mice to VT-2 and VT-1 was analyzed. Although wild-type mice died after administration of 0.02 microg of VT-2 or 1.0 microg of VT-1, the mutant mice showed no reaction to doses as much as 100 times that administered to wild types. Expression analysis of Gb3/CD77 in mouse tissues with antibody revealed that low, but definite, levels of Gb3/CD77 were expressed in the microvascular endothelial cells of the brain cortex and pia mater and in renal tubular capillaries. Corresponding to the Gb3/CD77 expression, tissue damage with edema, congestion, and cytopathic changes was observed, indicating that Gb3/CD77 (and its derivatives) exclusively function as a receptor for VTs in vivo. The lethal kinetics were similar regardless of lipopolysaccharide elimination in VT preparation, suggesting that basal Gb3/CD77 levels are sufficient for lethal effects of VTs.

Pubmed ID: 16476743


  • Okuda T
  • Tokuda N
  • Numata S
  • Ito M
  • Ohta M
  • Kawamura K
  • Wiels J
  • Urano T
  • Tajima O
  • Furukawa K
  • Furukawa K


The Journal of biological chemistry

Publication Data

April 14, 2006

Associated Grants


Mesh Terms

  • Animals
  • Blotting, Northern
  • Blotting, Southern
  • Brain
  • Chromatography, Thin Layer
  • Cytokines
  • Escherichia coli
  • Female
  • Galactosyltransferases
  • Gene Deletion
  • Gene Expression Regulation
  • Gene Expression Regulation, Enzymologic
  • Genetic Vectors
  • Glycolipids
  • Glycosphingolipids
  • Immunohistochemistry
  • Inflammation
  • Interleukin-1
  • Kidney
  • Kidney Tubules
  • Kinetics
  • Lipopolysaccharides
  • Lymphocytes
  • Male
  • Mice
  • Mice, Knockout
  • Microcirculation
  • Models, Genetic
  • Mutation
  • Recombination, Genetic
  • Reverse Transcriptase Polymerase Chain Reaction
  • Shiga Toxins
  • Time Factors
  • Tumor Necrosis Factor-alpha