Secreted Aspartyl Proteinases and Interactions of Candida albicans with Human Endothelial Cells
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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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Different attributes, including adhesion factors, the yeast-to-hyphal transition and hydrolytic enzyme secretion, are necessary for penetration of C. albicans through epithelial and endothelial layers.
“Different attributes, among which are adhesion factors, the yeast-to-hyphal transition and hydrolytic enzyme secretion, are necessary for penetration of C. albicans through the epithelial and endothelial layers (Hube et al ., 1997;Sanglard et al ., 1997;Ibrahim et al ., 1998;Brown and Gow, 1999;Sundstrom, 1999;Ernst, 2000;Phan et al ., 2000;Felk et al ., 2002).”
From Stage‐specific gene expression of <i>Candida albicans</i> in human blood (2003) · cites this paper as Ibrahim et al., 1998
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- Authors
- Ibrahim, A. S., Filler, S. G., Sanglard, D., Edwards, J. E., & Hube, B.
- Affiliations
- University of California, Los Angeles (US)
- Centre Hospitalier Universitaire Vaudois (CH)
- Universität Hamburg (DE)
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 1998-06
- Volume
- 66
- Issue
- 6
- Pages
- 3003-3005
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC108304
- OpenAlex
- W1838815905
- Cited by
- 62
- References
- 15
- Citations by year
- 2026: 2 · 2025: 2 · 2023: 2 · 2021: 1 · 2017: 1 · 2015: 1 · 2014: 1 · 2013: 1
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- American Heart Association
- Toyota USA
- National Institutes of Health (RR00425)
- National Institute of Allergy and Infectious Diseases (R01AI019990, P01AI037194)
- National Center for Research Resources (MO1-RR00425, M01RR000425)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, secreted aspartyl proteinases, SAP-1, SAP2, endothelial cells, fungal adhesion, endothelial injury, knockout mutants
- MeSH terms
- Candida albicans, Cell Adhesion, Endothelium, Vascular, Fungal Proteins, Humans, Aspartic Acid Endopeptidases, E-Selectin
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