The endothelial cell interactions of homozygous null mutants of Candida albicans that were deficient in secreted aspartyl proteinase 1 (Sap1), Sap2, or Sap3 were investigated. Only Sap2 was found to contribute to the ability of C. albicans to damage endothelial cells and stimulate them to express E-selectin. None of the Saps studied appears to play a role in C. albicans adherence to endothelial cells.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108304 | PMC |
| http://dx.doi.org/10.1128/IAI.66.6.3003-3005.1998 | DOI Listing |
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