Evidence map›Paper›PMID 35819969›Full record

ArticlePloS one2022

Mechanisms of azole antifungal resistance in clinical isolates of Candida tropicalis.

Saikat Paul, Dipika Shaw, Himanshu Joshi, Shreya Singh, Arunaloke Chakrabarti, Shivaprakash M Rudramurthy, Anup K Ghosh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Persistent Non-Journal of fungi (Basel, Switzerland) · 2026
    Article
  2. Article
  3. Article
  4. Mechanism of azole resistance inJournal of medical microbiology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Fluconazole resistance amongFrontiers in fungal biology · 2025
    Article
  13. Azole Resistance andJournal of fungi (Basel, Switzerland) · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Saikat PaulDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Dipika ShawDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Himanshu JoshiDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Shreya SinghDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Arunaloke ChakrabartiDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Shivaprakash M RudramurthyDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.ORCID 0000-0002-9097-9253
Anup K GhoshDepartment of Medical Microbiology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.ORCID 0000-0002-0341-6680
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was designed to understand the molecular mechanisms of azole resistance in Candida tropicalis using genetic and bioinformatics approaches. Thirty-two azole-resistant and 10 azole-susceptible (S) clinical isolates of C. tropicalis were subjected to mutation analysis of the azole target genes including ERG11. Inducible expression analysis of 17 other genes potentially associated with azole resistance was also evaluated. Homology modeling and molecular docking analysis were performed to study the effect of amino acid alterations in mediating azole resistance. Of the 32 resistant isolates, 12 (37.5%) showed A395T and C461T mutations in the ERG11 gene. The mean overexpression of CDR1, CDR3, TAC1, ERG1, ERG2, ERG3, ERG11, UPC2, and MKC1 in resistant isolates without mutation (R-WTM) was significantly higher (p<0.05) than those with mutation (R-WM) and the sensitive isolates (3.2-11 vs. 0.2-2.5 and 0.3-2.2 folds, respectively). Although the R-WTM and R-WM had higher (p<0.05) CDR2 and MRR1 expression compared to S isolates, noticeable variation was not seen among the other genes. Protein homology modelling and molecular docking revealed that the mutations in the ERG11 gene were responsible for structural alteration and low binding efficiency between ERG11p and ligands. Isolates with ERG11 mutations also presented A220C in ERG1 and together T503C, G751A mutations in UPC2. Nonsynonymous mutations in the ERG11 gene and coordinated overexpression of various genes including different transporters, ergosterol biosynthesis pathway, transcription factors, and stress-responsive genes are associated with azole resistance in clinical isolates of C. tropicalis.

Indexed as

AzolesCandida tropicalisAntifungal AgentsMicrobial Sensitivity TestsMolecular Docking SimulationAntifungal AgentsAzoles

Identifiers

PMID35819969
PMCPMC9275685
OpenAlexW4285079062

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Registered trials

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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.