Evidence map›Paper›PMID 23229483›Full record

ArticleAntimicrobial agents and chemotherapy2013

STB5 is a negative regulator of azole resistance in Candida glabrata.

Jason A Noble, Huei-Fung Tsai, Sara D Suffis, Qin Su, Timothy G Myers, John E Bennett

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. mSphere · 2024
    Article
  3. Article
  4. Multiple genome analysis ofMicrobial cell (Graz, Austria) · 2022
    Article
  5. Article
  6. Loss-of-FunctionmSphere · 2021
    Article
  7. Article
  8. Fungal Zn(II)Antimicrobial agents and chemotherapy · 2021
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Candida glabrata Biofilms: How Far Have We Come?Journal of fungi (Basel, Switzerland) · 2017
    Review
  16. Azole Resistance in Candida glabrata.Current infectious disease reports · 2016
    Review
  17. Article
  18. Membrane Proteomics Analysis of theFrontiers in microbiology · 2016
    Article
  19. Review
  20. Article
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

6 authors at 2 institutions in 1 country.

Jason A NobleClinical Mycology Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Huei-Fung Tsai
Sara D Suffis
Qin Su
Timothy G Myers
John E Bennett
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Infectious Diseases Research Technologies Core - BethesdaZICAI001051 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$226.1M
Molecular Genetics, Biochemistry And Therapy Of Pathogenic FungiZIAAI000654 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BENNETT, JOHN E · 2009 to 2014
$3.4M
Intramural NIH HHS
6 · The paper itself

Abstract

The opportunistic yeast pathogen Candida glabrata is recognized for its ability to acquire resistance during prolonged treatment with azole antifungals (J. E. Bennett, K. Izumikawa, and K. A. Marr. Antimicrob. Agents Chemother. 48:1773-1777, 2004). Resistance to azoles is largely mediated by the transcription factor PDR1, resulting in the upregulation of ATP-binding cassette (ABC) transporter proteins and drug efflux. Studies in the related yeast Saccharomyces cerevisiae have shown that Pdr1p forms a heterodimer with another transcription factor, Stb5p. In C. glabrata, the open reading frame (ORF) designated CAGL0I02552g has 38.8% amino acid identity with STB5 (YHR178w) and shares an N-terminal Zn(2)Cys(6) binuclear cluster domain and a fungus-specific transcriptional factor domain, prompting us to test for homologous function and a possible role in azole resistance. Complementation of a Δyhr178w (Δstb5) mutant with CAGL0I02552g resolved the increased sensitivity to cold, hydrogen peroxide, and caffeine of the mutant, for which reason we designated CAGl0I02552g CgSTB5. Overexpression of CgSTB5 in C. glabrata repressed azole resistance, whereas deletion of CgSTB5 caused a modest increase in resistance. Expression analysis found that CgSTB5 shares many transcriptional targets with CgPDR1 but, unlike the latter, is a negative regulator of pleiotropic drug resistance, including the ABC transporter genes CDR1, PDH1, and YOR1.

Indexed as

Amino Acid SequenceAntifungal AgentsATP-Binding Cassette TransportersAzolesCandida glabrataDNA-Binding ProteinsDrug Resistance, FungalFluconazoleFungal ProteinsGene DeletionGene Expression Regulation, FungalMicrobial Sensitivity TestsMolecular Sequence DataMutationOxidative StressPyrimidinesAntifungal AgentsATP-Binding Cassette TransportersAzolesDNA-Binding ProteinsFluconazoleFungal ProteinsPDR1 protein, S cerevisiaePyrimidinesSaccharomyces cerevisiae ProteinsStb5 protein, S cerevisiaeTranscription FactorsTriazolesVoriconazole

Identifiers

PMID23229483
PMCPMC3553707
OpenAlexW2104744906

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.