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Literature summary for 3.4.24.81 extracted from

  • Powers, M.; Kim, H.; Wang, Y.; Wardenburg, J.
    ADAM10 mediates vascular injury induced by Staphylococcus aureus alpha-hemolysin (2012), J. Infect. Dis., 206, 352-356.
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
medicine Staphylococcus aureus alpha-hemolysin, a pore-forming cytotoxin, is required for full virulence in a murine sepsis model. The alpha-hemolysin binding to its receptor A-disintegrin and metalloprotease ADAM10 upregulates the receptor’s metalloprotease activity on endothelial cells, causing vascular endothelial-cadherin cleavage and concomitant loss of endothelial barrier function Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
GI254023X
-
 Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus O35598
-
-

General Information

General Information Comment Organism
physiological function Staphylococcus aureus alpha-hemolysin, a pore-forming cytotoxin, is required for full virulence in a murine sepsis model. The alpha-hemolysin binding to its receptor A-disintegrin and metalloprotease ADAM10 upregulates the receptor's metalloprotease activity on endothelial cells, causing vascular endothelial-cadherin cleavage and concomitant loss of endothelial barrier function Mus musculus