ArticleAntimicrobial agents and chemotherapy2015
In Vitro Biochemical Study of CYP51-Mediated Azole Resistance in Aspergillus fumigatus.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- A long noncoding RNA regulates in vitro and in vivo triazole antifungal susceptibility in Aspergillus fumigatus.Genetics · 2026Article
- Agricultural fungicides shape soil and sediment reservoirs of multidrug-resistant fungi.Nature communications · 2026Article
- A long non-coding RNA regulates triazole antifungal susceptibility and virulence inbioRxiv : the preprint server for biology · 2025Article
- Itraconazole resistance in Madurella fahalii linked to a distinct homolog of the gene encoding cytochrome P450 14-α sterol demethylase (CYP51).PLoS neglected tropical diseases · 2025Article
- Understanding the clinical and environmental drivers of antifungal resistance in the One Health context.Microbiology (Reading, England) · 2024Review
- Drug-ResistantPathogens (Basel, Switzerland) · 2023Review
- Analysis of theAntimicrobial agents and chemotherapy · 2023Article
- Azole Resistance-Associated Regulatory Motifs within the Promoter ofMicrobiology spectrum · 2022Article
- The Caspofungin Paradoxical Effect is a Tolerant "Eagle Effect" in the Filamentous Fungal PathogenmBio · 2022Article
- Recent Molecular Tools for the Genetic Manipulation of Highly Industrially Important Mucoromycota Fungi.Journal of fungi (Basel, Switzerland) · 2021Review
- Recent Advances in Genome Editing Tools in Medical Mycology Research.Journal of fungi (Basel, Switzerland) · 2021Review
- A Simple Method To Detect Point Mutations in Aspergillus fumigatusAntimicrobial agents and chemotherapy · 2020Article
- Genome-Wide Association for Itraconazole Sensitivity in Non-resistant Clinical Isolates ofFrontiers in fungal biology · 2020Article
- New Insights into the Cyp51 Contribution to Azole Resistance inAntimicrobial agents and chemotherapy · 2019Article
- Mutations inmBio · 2019Article
- Emerging threat of triazole-resistant Aspergillus fumigatus.The Journal of antimicrobial chemotherapy · 2019Review
- Non-cyp51A Azole-Resistant Aspergillus fumigatus Isolates with Mutation in HMG-CoA Reductase.Emerging infectious diseases · 2018Article
- Article
- Impact of Homologous Resistance Mutations from Pathogenic Yeast on Saccharomyces cerevisiae Lanosterol 14α-Demethylase.Antimicrobial agents and chemotherapy · 2018Article
- Molecular Tools for the Detection and Deduction of Azole Antifungal Drug Resistance Phenotypes in Aspergillus Species.Clinical microbiology reviews · 2017Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of triazole-resistant Aspergillus infections is increasing worldwide, often mediated through mutations in the CYP51A amino acid sequence. New classes of azole-based drugs are required to combat the increasing resistance to existing triazole therapeutics. In this study, a CYP51 reconstitution assay is described consisting of eburicol, purified recombinant Aspergillus fumigatus CPR1 (AfCPR1), and Escherichia coli membrane suspensions containing recombinant A. fumigatus CYP51 proteins, allowing in vitro screening of azole antifungals. Azole-CYP51 studies determining the 50% inhibitory concentration (IC50) showed that A. fumigatus CYP51B (Af51B IC50, 0.50 μM) was 34-fold more susceptible to inhibition by fluconazole than A. fumigatus CYP51A (Af51A IC50, 17 μM) and that Af51A and Af51B were equally susceptible to inhibition by voriconazole, itraconazole, and posaconazole (IC50s of 0.16 to 0.38 μM). Af51A-G54W and Af51A-M220K enzymes were 11- and 15-fold less susceptible to inhibition by itraconazole and 30- and 8-fold less susceptible to inhibition by posaconazole than wild-type Af51A, confirming the azole-resistant phenotype of these two Af51A mutations. Susceptibility to voriconazole of Af51A-G54W and Af51A-M220K was only marginally lower than that of wild-type Af51A. Susceptibility of Af51A-L98H to inhibition by voriconazole, itraconazole, and posaconazole was only marginally lower (less than 2-fold) than that of wild-type Af51A. However, Af51A-L98H retained 5 to 8% residual activity in the presence of 32 μM triazole, which could confer azole resistance in A. fumigatus strains that harbor the Af51A-L98H mutation. The AfCPR1/Af51 assay system demonstrated the biochemical basis for the increased azole resistance of A. fumigatus strains harboring G54W, L98H, and M220K Af51A point mutations.
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