ArticleAntimicrobial agents and chemotherapy2014
Identification of genomic binding sites for Candida glabrata Pdr1 transcription factor in wild-type and ρ0 cells.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Facile generation ofMicrobiology spectrum · 2026Article
- Tn-seq screens inmSphere · 2025Article
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- Overlapping coactivator function is required for transcriptional activation by the Candida glabrata Pdr1 transcription factor.Genetics · 2024Article
- Transposon-sequencing (Tn-seq) of the Candida glabrata reference strain CBS138 reveals epigenetic plasticity, structural variation, and intrinsic mechanisms of resistance to micafungin.G3 (Bethesda, Md.) · 2024Article
- Review
- Interactions between the transcription factors FfmA and AtrR are required to properly regulate gene expression in the fungus Aspergillus fumigatus.G3 (Bethesda, Md.) · 2023Article
- Redefining pleiotropic drug resistance in a pathogenic yeast: Pdr1 functions as a sensor of cellular stresses inmSphere · 2023Article
- Transcription factor FfmA interacts both physically and genetically with AtrR to properly regulate gene expression in the fungusbioRxiv : the preprint server for biology · 2023Article
- Characterizing Candida glabrata Pdr1, a Hyperactive Transcription Factor Involved in Azole Resistance.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Characterization of theJournal of fungi (Basel, Switzerland) · 2022Article
- Loss-of-FunctionmSphere · 2021Article
- The Candida glabrata Upc2A transcription factor is a global regulator of antifungal drug resistance pathways.PLoS genetics · 2021Article
- Antifungal Drug Resistance: Molecular Mechanisms inChemical reviews · 2021Review
- Identification of Essential Genes and Fluconazole Susceptibility Genes inG3 (Bethesda, Md.) · 2020Article
- Functional information from clinically-derived drug resistant forms of the Candida glabrata Pdr1 transcription factor.PLoS genetics · 2020Article
- Screening the Drug:HFrontiers in cellular and infection microbiology · 2020Article
- Article
- Article
- Multiple interfaces control activity of the Candida glabrata Pdr1 transcription factor mediating azole drug resistance.Current genetics · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The fungal pathogen Candida glabrata is an emerging cause of candidiasis in part owing to its robust ability to acquire tolerance to the major clinical antifungal drug fluconazole. Similar to the related species Candida albicans, C. glabrata most typically gains azole tolerance via transcriptional induction of a suite of resistance genes, including a locus encoding an ABCG-type ATP-binding cassette (ABC) transporter that is referred to as CDR1 in Candida species. In C. glabrata, CDR1 expression is controlled primarily by the activity of a transcriptional activator protein called Pdr1. Strains exhibiting reduced azole susceptibility often contain substitution mutations in PDR1 that in turn lead to elevated mRNA levels of target genes with associated azole resistance. Pdr1 activity is also induced upon loss of the mitochondrial genome status and upon challenge by azole drugs. While extensive analyses of the transcriptional effects of Pdr1 have identified a number of genes that are regulated by this factor, we cannot yet separate direct from indirect target genes. Here we used chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) to identify the promoters and associated genes directly regulated by Pdr1. These genes include many that are shared with the yeast Saccharomyces cerevisiae but others that are unique to C. glabrata, including the ABC transporter-encoding locus YBT1, genes involved in DNA repair, and several others. These data provide the outline for understanding the primary response genes involved in production of Pdr1-dependent azole resistance in C. glabrata.
Indexed as
Identifiers
What OpenQuestion holds
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.