ArticleThe Journal of biological chemistry2014
The peptide-binding cavity is essential for Als3-mediated adhesion of Candida albicans to human cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 85 citations in OpenAlex.
- Review
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- mGem: Fungal adhesins inmBio · 2026Article
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- MUC16-dependent Renal Vascular Adhesion of Candida Promotes Tissue Invasion and Predicts Clinical Outcome in Candidemia.Research square · 2026Article
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- Functional Amyloids in Adhesion of Non-Pathogens (Basel, Switzerland) · 2025Article
- Review
- Development of Miniprotein-Type Inhibitors of Biofilm Formation inJournal of microbiology and biotechnology · 2025Article
- Fungal Als proteins hijack host death effector domains to promote inflammasome signaling.Nature communications · 2025Article
- Article
- Hyphal Als proteins act as CR3 ligands to promote immune responses against Candida albicans.Nature communications · 2024Article
- Promising immunotherapeutic targets for treating candidiasis.Frontiers in cellular and infection microbiology · 2024Review
- Use of aFrontiers in cellular and infection microbiology · 2024Article
- Surface adherence and vacuolar internalization of bacterial pathogens to the Candida spp. cells: Mechanism of persistence and propagation.Journal of advanced research · 2023Review
- Exploration of Baicalein-Core Derivatives as Potent Antifungal Agents: SAR and Mechanism Insights.Molecules (Basel, Switzerland) · 2023Article
- The catheterized bladder environment promotes Efg1- and Als1-dependentScience advances · 2023Article
- Gold Nanoparticle-Based Therapy for Muscle Inflammation and Oxidative Stress.Journal of inflammation research · 2022Review
- Assessing Als3 Peptide-Binding Cavity and Amyloid-Forming Region Contributions toFrontiers in cellular and infection microbiology · 2022Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The adhesive phenotype of Candida albicans contributes to its ability to colonize the host and cause disease. Als proteins are one of the most widely studied C. albicans virulence attributes; deletion of ALS3 produces the greatest reduction in adhesive function. Although adhesive activity is thought to reside within the N-terminal domain of Als proteins (NT-Als), the molecular mechanism of adhesion remains unclear. We designed mutations in NT-Als3 that test the contribution of the peptide-binding cavity (PBC) to C. albicans adhesion and assessed the adhesive properties of other NT-Als3 features in the absence of a functional PBC. Structural analysis of purified loss-of-PBC-function mutant proteins showed that the mutations did not alter the overall structure or surface properties of NT-Als3. The mutations were incorporated into full-length ALS3 and integrated into the ALS3 locus of a deletion mutant, under control of the native ALS3 promoter. The PBC mutant phenotype was evaluated in assays using monolayers of human pharyngeal epithelial and umbilical vein endothelial cells, and freshly collected human buccal epithelial cells in suspension. Loss of PBC function resulted in an adhesion phenotype that was indistinguishable from the Δals3/Δals3 strain. The adhesive contribution of the Als3 amyloid-forming-region (AFR) was also tested using these methods. C. albicans strains producing cell surface Als3 in which the amyloidogenic potential was destroyed showed little contribution of the AFR to adhesion, instead suggesting an aggregative function for the AFR. Collectively, these results demonstrate the essential and principal role of the PBC in Als3 adhesion.
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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.