ArticleAntimicrobial agents and chemotherapy2005
Small-molecule inhibitors of the budded-to-hyphal-form transition in the pathogenic yeast Candida albicans.
Article in Antimicrobial agents and chemotherapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 71 citations in OpenAlex.
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- Synergistic Antibiofilm Effects of Pseudolaric Acid A Combined with Fluconazole against Candida albicans via Inhibition of Adhesion and Yeast-To-Hypha Transition.Microbiology spectrum · 2022Article
- Repurposing the FDA-approved anticancer agent ponatinib as a fluconazole potentiator by suppression of multidrug efflux and Pma1 expression in a broad spectrum of yeast species.Microbial biotechnology · 2022Article
- CouldJournal of clinical medicine · 2022Review
- Comprehensive genetic analysis of adhesin proteins and their role in virulence of Candida albicans.Genetics · 2021Article
- Mechanistic Understanding ofFrontiers in microbiology · 2021Review
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- Inhibition of Distinct Proline- orBioMed research international · 2020Article
- Antibiotic-induced gut metabolome and microbiome alterations increase the susceptibility to Candida albicans colonization in the gastrointestinal tract.FEMS microbiology ecology · 2020Article
- Linking Cellular Morphogenesis with Antifungal Treatment and Susceptibility inJournal of fungi (Basel, Switzerland) · 2019Review
- Two New 1,3,4-Oxadiazoles With Effective Antifungal Activity AgainstFrontiers in microbiology · 2019Article
- A phenotypic small-molecule screen identifies halogenated salicylanilides as inhibitors of fungal morphogenesis, biofilm formation and host cell invasion.Scientific reports · 2018Article
- Inhibition of yeast-to-filamentous growth transitions in Candida albicans by a small molecule inducer of mammalian apoptosis.Yeast (Chichester, England) · 2018Article
- Chemical inhibitors of Candida albicans hyphal morphogenesis target endocytosis.Scientific reports · 2017Article
- Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The pathogenic yeast Candida albicans can exist in multiple morphological states, including budded, pseudohyphal, and true hyphal forms. The ability to convert between the budded and hyphal forms, termed the budded-to-hyphal-form transition, is important for virulence and is regulated by multiple environmental and cellular signals. To identify inhibitors of this morphological transition, a microplate-based morphological assay was developed. With this assay, the known actin-inhibiting drugs latrunculin-A and jasplakinolide were shown to inhibit the transition in a dose-dependent and reversible manner. Five novel small molecules that reversibly inhibited the transition and hyphal elongation without affecting budded growth were identified. These molecules inhibited hyphal growth induced by Spider, Lee's, M199 pH 8, and 10% serum-containing media, with two molecules having a synergistic effect. The molecules also differentially affected the hyphal form-specific gene expression of HWP1 and endocytosis without disrupting the actin cytoskeleton or septin organization. Structural derivatives of one of the molecules were more effective inhibiters than the original molecule, while other derivatives had decreased efficacies. Several of the small molecules were able to reduce C. albicans-dependent damage to endothelial cells by inhibiting the budded-to-hyphal-form transition. These studies substantiated the effectiveness of the morphological assay and identified several novel molecules that, by virtue of their ability to inhibit the budded-to-hyphal-form transition, may be exploited as starting points for effective antifungal therapeutics in the future.
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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.