Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Gain of function mutations in CgPDR1 of Candida glabrata not only mediate antifungal resistance but also enhance virulence.

PLoS pathogens - 1 Jan 2009

Ferrari Sélène, Ischer Françoise, Calabrese David, Posteraro Brunella, Sanguinetti Maurizio, Fadda Giovanni, Rohde Bettina, Bauser Christopher, Bader Oliver, Sanglard Dominique

Abstract excerpt

CgPdr1p is a Candida glabrata Zn(2)-Cys(6) transcription factor involved in the regulation of the ABC-transporter genes CgCDR1, CgCDR2, and CgSNQ2, which are mediators of azole resistance. Single-point mutations in CgPDR1 are known to increase the expression of at least CgCDR1 and CgCDR2 and thus to contribute to azole resistance of clinical isolates. In this study, we investigated the incidence of CgPDR1...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to ATP-Binding Cassette Transporters
Share to Candida glabrata

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Candidiasis

Share to Drug Resistance, Fungal

Share to Fluconazole

Share to Gene Expression Regulation, Fungal

Share to Mice, Inbred BALB C

Share to Virulence

Source

Open in PubMed Open full text

Identifiers

PMID: 19148266
DOI: 10.1371/journal.ppat.1000268
PMCID: PMC2607542

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Gain of function mutations in CgPDR1 of Candida glabrata not only mediate antifungal resistance but also enhance virulence.PMID 19148266Read ↗

Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata.Semantic proximity Read ↗

Disclosing azole resistance mechanisms in resistant Candida glabrata strains encoding wild-type or gain-of-function CgPDR1 alleles through comparative genomics and transcriptomics.Semantic proximity Read ↗

Cg PDR 1 gain‐of‐function mutations lead to azole‐resistance and increased adhesion in clinical Candida glabrata strainsSemantic proximity Read ↗

Gain-of-Function Mutations in <i>PDR1</i> , a Regulator of Antifungal Drug Resistance in Candida glabrata, Control Adherence to Host CellsSemantic proximity Read ↗

Genomewide Expression Profile Analysis of the Candida glabrata Pdr1 RegulonSemantic proximity Read ↗

Candida glabrata PDR1 , a Transcriptional Regulator of a Pleiotropic Drug Resistance Network, Mediates Azole Resistance in Clinical Isolates and Petite MutantsSemantic proximity Read ↗

Multiple genome analysis of Candida glabrata clinical isolates renders new insights into genetic diversity and drug resistance determinantsSemantic proximity Read ↗

Comparative genomic and transcriptomic analyses unveil novel features of azole resistance and adaptation to the human host in Candida glabrata.Semantic proximity Read ↗

Functional information from clinically-derived drug resistant forms of the Candida glabrata Pdr1 transcription factorSemantic proximity Read ↗

Positive autoregulation and repression of transactivation are key regulatory features of the Candida glabrata Pdr1 transcription factorSemantic proximity Read ↗

Two Functionally Redundant FK506-Binding Proteins Regulate Multidrug Resistance Gene Expression and Govern Azole Antifungal ResistanceSemantic proximity Read ↗

A homologous overexpression system to study roles of drug transporters in Candida glabrata.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.