• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

Authors

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

Journal

The Journal of biological chemistry

Publication Data

April 14, 2006

Associated Grants

None

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