ArticleInfection and immunity1997
Disruption of each of the secreted aspartyl proteinase genes SAP1, SAP2, and SAP3 of Candida albicans attenuates virulence.
Article in Infection and immunity, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
108 citing papers in PubMed, 315 citations in OpenAlex.
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- Identification of a protective antigen reveals the trade-off between iron acquisition and antigen exposure in a global fungal pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Image-based quantification of Candida albicans filamentation and hyphal length using the open-source visual programming language JIPipe.FEMS yeast research · 2025Article
- The P-type calcium pump Spf1 regulates immune response by maintenance of the endoplasmic reticulum-plasma membrane contacts duringMycology · 2025Article
- Functional Characterization ofJournal of fungi (Basel, Switzerland) · 2024Article
- Saps1-3 Antigens inInfectious disease reports · 2024Article
- Secreted Aspartic Proteinases: Key Factors inInternational journal of molecular sciences · 2024Review
- Toll-like receptor 4 and CD11b expressed on microglia coordinate eradication of Candida albicans cerebral mycosis.Cell reports · 2023Article
- The Pathogenic YeastJournal of fungi (Basel, Switzerland) · 2023Review
- Morphogenic plasticity: the pathogenic attribute of Candida albicans.Current genetics · 2023Review
- Complete genome analysis of pathogenic Metschnikowia bicuspidata strain MQ2101 isolated from diseased ridgetail white prawn, Exopalaemon carinicauda.BMC microbiology · 2023Article
- Polyphyllin I EffectsEvidence-based complementary and alternative medicine : eCAM · 2023Article
- Secreted aspartyl protease 3 regulated by the Ras/cAMP/PKA pathway promotes the virulence ofFrontiers in cellular and infection microbiology · 2023Article
- Pathogenesis and virulence ofVirulence · 2022Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Secreted aspartyl proteinases (Saps), encoded by a gene family with at least nine members (SAP1 to SAP9), are one of the most discussed virulence factors produced by the human pathogen Candida albicans. In order to study the role of each Sap isoenzyme in pathogenicity, we have constructed strains which harbor mutations at selected SAP genes. SAP1, SAP2, and SAP3, which are regulated differentially in vitro, were mutated by targeted gene disruption. The growth rates of all homozygous null mutants were similar to those of the isogenic wild-type parental strain (SC5314) in complex and defined media. In medium with protein as the sole source of nitrogen, sap1 and sap3 mutants grew with reduced growth rates but reached optical densities similar to those measured for SC5314. In contrast, sap2 null mutants tended to clump, grew poorly in this medium, and produced the lowest proteolytic activity. Addition of ammonium ions reversed such growth defects. These results support the view that Sap2 is the dominant isoenzyme. When sap1, sap2, and sap3 mutants were injected intravenously in guinea pigs and mice, the animals had increased survival rates compared to those of control animals infected with SC5314. However, reduction of proteolytic activity in vitro did not correlate directly with the extent of attenuation of virulence observed for all Sap-deficient mutants. These data suggest that SAP1, SAP2, and SAP3 all contribute to the overall virulence of C. albicans and presumably all play important roles during disseminated infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.