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

An A643T mutation in the transcription factor Upc2p causes constitutive ERG11 upregulation and increased fluconazole resistance in Candida albicans.

Antimicrobial agents and chemotherapy - 1 Jan 2010

Heilmann Clemens J, Schneider Sabrina, Barker Katherine S, Rogers P David, Morschhäuser Joachim

Abstract excerpt

The zinc cluster transcription factor Upc2p mediates upregulation of ergosterol biosynthesis genes in response to ergosterol depletion in the fungal pathogen Candida albicans. One mechanism of acquired resistance to the antifungal drug fluconazole, which inhibits ergosterol biosynthesis, is constitutively increased expression of the ERG11 gene encoding the drug target enzyme. A G648D mutation in Upc2p has...

Read the complete abstract on PubMed

Topics

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

Share to Antifungal Agents
Share to Candida albicans

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Candidiasis

Share to Cytochrome P-450 Enzyme System

Share to DNA, Fungal

Share to Drug Resistance, Fungal

Share to Fluconazole

Share to Transformation, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 19884367
DOI: 10.1128/AAC.01102-09
PMCID: PMC2798556

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An A643T mutation in the transcription factor Upc2p causes constitutive ERG11 upregulation and increased fluconazole resistance in Candida albicans.PMID 19884367Read ↗

A gain-of-function mutation in the transcription factor Upc2p causes upregulation of ergosterol biosynthesis genes and increased fluconazole resistance in a clinical Candida albicans isolate.Semantic proximity Read ↗

Gain-of-Function Mutations in UPC2 Are a Frequent Cause of ERG11 Upregulation in Azole-Resistant Clinical Isolates of Candida albicansSemantic proximity Read ↗

Candida albicans zinc cluster protein Upc2p confers resistance to antifungal drugs and is an activator of ergosterol biosynthetic genes.Semantic proximity Read ↗

Role of Candida albicans transcription factor Upc2p in drug resistance and sterol metabolism.Semantic proximity Read ↗

Upc2p-associated differential protein expression in Candida albicans.Semantic proximity Read ↗

The Candida glabrata Upc2A transcription factor is a global regulator of antifungal drug resistance pathways.Semantic proximity Read ↗

An A643V Amino Acid Substitution in Upc2p Contributes to Azole Resistance in Well-Characterized Clinical Isolates of <i>Candida albicans</i>Semantic proximity Read ↗

Azole resistance is mediated by integration of sterol gene regulation and membrane transporter production by the zinc cluster-containing transcription factor Upc2A in <i>Candida glabrata</i>Semantic proximity Read ↗

Disruption of the <em>UPC2</em> Gene Enhances Fluconazole Antifungal Activity by Inhibiting <em>HAC1</em> mRNA Splicing in <em>Candida albicans</em>Semantic proximity Read ↗

cis-Acting elements within the Candida albicans ERG11 promoter mediate the azole response through transcription factor Upc2p.Semantic proximity Read ↗

Candida tropicalis distribution and drug resistance is correlated with ERG11 and UPC2 expressionSemantic proximity Read ↗

Nonidentical function of Upc2A binding sites in the Candida glabrata CDR1 promoterSemantic proximity Read ↗

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