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Links from GEO DataSets

Items: 20

1.

Loss of mitochondrial functions in Candida glabrata results in enhanced virulence in mice

(Submitter supplied) Two C. glabrata related isolates recovered from the same patient undergoing azole therapy were characterized. The first isolate, BPY40, is azole-susceptibleand the second, BPY41, is azole-resistant. To determine whether the petite mutation conferred a selective advantage during host infection, the virulence of BPY40 and BPY41 was assessed in mice. Surprisingly, the petite mutant, even if showing in vitro growth deficiency as compared to BPY40, was more virulent than BPY40 both in intravenous and vaginal murine infection models. more...
Organism:
Nakaseomyces glabratus; Nakaseomyces glabratus CBS 138
Type:
Expression profiling by array
Platform:
GPL10713
6 Samples
Download data: TXT
Series
Accession:
GSE23826
ID:
200023826
2.

Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Nakaseomyces glabratus CBS 138; Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL10713
33 Samples
Download data: TXT
Series
Accession:
GSE23829
ID:
200023829
3.

Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata (part 2)

(Submitter supplied) In this study, we aimed to determine genome-wide changes in gene expression driven by seven individual CgPDR1 hyperactive alleles as compared to wild-type allele to identify i) the CgPdr1p target genes differentially expressed in presence of CgPDR1 hyperactive alleles and ii) potential virulence factor(s) regulated by CgPDR1 hyperactive alleles. Microarray experiments revealed a high number of genes (ranging from 80 to 400 genes) differentially regulated by individual CgPDR1 hyperactive alleles.
Organism:
Nakaseomyces glabratus; Nakaseomyces glabratus CBS 138
Type:
Expression profiling by array
Platform:
GPL10713
6 Samples
Download data: TXT
Series
Accession:
GSE23828
ID:
200023828
4.

Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata (part 1)

(Submitter supplied) In this study, we aimed to determine genome-wide changes in gene expression driven by seven individual CgPDR1 hyperactive alleles as compared to wild-type allele to identify i) the CgPdr1p target genes differentially expressed in presence of CgPDR1 hyperactive alleles and ii) potential virulence factor(s) regulated by CgPDR1 hyperactive alleles. Microarray experiments revealed a high number of genes (ranging from 80 to 400 genes) differentially regulated by individual CgPDR1 hyperactive alleles.
Organism:
Nakaseomyces glabratus CBS 138; Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL10713
27 Samples
Download data: TXT
Series
Accession:
GSE23827
ID:
200023827
5.

Milbemycins: more than efflux inhibitors for fungal pathogens

(Submitter supplied) This study investigated the effect of milbemycons as efflux inhibitors and antifungal agents. Milbemycin oxims can inhibit growth of Candida glabrata and C. albicans. The effect of milbemycins on transcriptomes was inbvestigated.
Organism:
Nakaseomyces glabratus CBS 138; Candida albicans; Nakaseomyces glabratus
Type:
Expression profiling by array
Platforms:
GPL10713 GPL15960
14 Samples
Download data: TXT
Series
Accession:
GSE40232
ID:
200040232
6.

Azole Resistance Mechanism in Candida glabrata

(Submitter supplied) Microarray was used to analyze azole resistance of Candida glabrata oropharyngeal isolates from 7 hematopoietic stem cell transplant recipients receiving fluconazole prophylaxis. Transcriptional profiling of the sequential-paired clinical isolates by microarray revealed 19 genes upregulated in the majority of resistant isolates compared to their paired-susceptible isolates. All seven resistant isolates had greater than two fold upregulation of CgPDR1, a master transcriptional regulator of PDR network, and all 7 resistant isolates showed upregulation of known CgPDR1-target genes. more...
Organism:
Nakaseomyces glabratus CBS 138; Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL10325
8 Samples
Download data: TXT
Series
Accession:
GSE21355
ID:
200021355
7.

Azole Resistance Mechanism in Candida glabrata Oropharyngeal Isolates

(Submitter supplied) Microarray was used to analyze azole resistance of Candida glabrata oropharyngeal isolates from 7 hematopoietic stem cell transplant recipients receiving fluconazole prophylaxis. Transcriptional profiling of the sequential-paired clinical isolates by microarray revealed 19 genes upregulated in the majority of resistant isolates compared to their paired-susceptible isolates. All seven resistant isolates had greater than two fold upregulation of CgPDR1, a master transcriptional regulator of PDR network, and all 7 resistant isolates showed upregulation of known CgPDR1-target genes. more...
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL8174
35 Samples
Download data: GPR
Series
Accession:
GSE21352
ID:
200021352
8.

The Candida glabrata transcription factor Stb5p is a negative regulator of ATP-binding cassette transporters

(Submitter supplied) The opportunistic yeast pathogen Candida glabrata is recognized for its ability to acquire resistance during prolonged treatment with azole antifungals. 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 Pdr1p forms a heterodimer with another transcription factor, Stb5p. more...
Organism:
Nakaseomyces glabratus; Nakaseomyces glabratus CBS 138
Type:
Expression profiling by array
Platforms:
GPL8174 GPL10325
13 Samples
Download data: GPR, TXT
Series
Accession:
GSE37071
ID:
200037071
9.

Exploring comparative and transcriptomic analyses to unveil mechanisms of resistance to azoles dependent and independent of CgPdr1 in Candida glabrata clinical isolates

(Submitter supplied) The pathogenic yeast species Candida glabrata has an intrinsically high resilience to azoles and a rapid capability of acquiring resistance. Azole-resistant clinical strains derive mostly from them encoding hyperactive mutants of the CgPdr1 regulator, however, strains encoding wild-type CgPdr1 variants were identified suggesting a role for CgPdr1-independent mechanisms in acquisition of resistance in vivo. more...
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL29725
14 Samples
Download data: TXT, XLS
Series
Accession:
GSE166841
ID:
200166841
10.

Genomic level analysis of Upc2A-regulated transcription in Candida glabrata

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Nakaseomyces glabratus CBS 138; Nakaseomyces glabratus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL22622 GPL30531
28 Samples
Download data: BIGWIG, WIG
Series
Accession:
GSE182516
ID:
200182516
11.

RNA-seq Analysis of Wild-Type and G898D UPC2A Transcriptomes [G898D UPC2A transcriptome]

(Submitter supplied) Purpose: Determine the number of genes that respond to the presence of a gain-of-function mutant form of the UPC2A transcription factor in Candida glabrata. Methods: Prepare total RNA from wild-type and gain-of-function G898D UPC2A cells. Use standard RNA-seq to evaluate and compare the transcriptomic changes caused by this allele of UPC2A. Results: Although a clear increase was seen in fluconazole resistance conferred by the G898D UPC2A allele, elevated transcription was only observed for 11 genes with 9 of these involved in ergosterol biosynthesis. more...
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL22622
6 Samples
Download data: BIGWIG
Series
Accession:
GSE182490
ID:
200182490
12.

RNA-sequencing analysis of fluconazole-treated wild-type and upc2A null cells [Fluconazole]

(Submitter supplied) Purpose: Compare the fluconazole-induced transcriptome of isogenic wild-type and upc2A null cells. Methods: Prepare total RNA from wild-type and upc2A null cells grown under unstressed conditions or challenged with 50 microgram/ml fluconazole for 6 hours. Use standard RNA-seq to evaluate and compare the transcriptomic changes caused by fluconazole in the presence or absence of UPC2A. Results: These data established that over 100 genes were induced by fluconazole in a UPC2A-dependent manner. more...
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL22622
12 Samples
Download data: WIG
Series
Accession:
GSE182489
ID:
200182489
13.

ChIP-seq analysis of transcription factor Upc2A binding across the Candida glabrata genome [Upc2A ChIP-seq]

(Submitter supplied) To determine the genomic binding sites for the Candida glabrata transcription factor Upc2A, we utilized three different strains. One was the wild-type KKY2001 which contains a wild-type copy of UPC2A but lacks any HA tag. The other two are both derived from KKY2001 but contain a 3X HA tag immediately after the start codon of UPC2A. These strains are BVGC82 and BVGC84, respectively. Both contain a single copy of a loxP element located 252 bp downstream from the UPC2A stop codon. more...
Organism:
Nakaseomyces glabratus CBS 138
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30531
10 Samples
Download data: WIG
Series
Accession:
GSE182488
ID:
200182488
14.

Genome-wide expression profile analysis of the Candida glabrata Pdr1 regulon

(Submitter supplied) The ABC-transporters CgCdr1, CgPdh1, and CgSnq2 are known to mediate azole resistance in the pathogenic fungus Candida glabrata. Activating mutations in CgPDR1, a zinc cluster transcription factor, result in constitutive up-regulation of these ABC-transporter genes but to varying degrees. We examined the genome-wide gene expression profiles of two matched azole-susceptible and –resistant C. glabrata clinical isolate pairs. more...
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by array
Platform:
GPL10870
16 Samples
Download data: CEL
Series
Accession:
GSE24168
ID:
200024168
15.

Genomic targets sites of the Candida glabrata transcription factor Pdr1

(Submitter supplied) Pdr1 is the major regulator of azole resistance in the fungal pathogen Candida glabrata. Earlier experiments demonstrated that expression of Pdr1 itself is increased when cells lose their mitochondrial genome (rho0). Here we use chromatin immunoprecipitation coupled with highthroughput sequencing (ChIP-seq) to map the genomic binding sites for Pdr1 in both normal and rho0 cells. These data provide the first look at genes that are likely to represent the direct targets of Pdr1 in this important pathogen.
Organism:
Nakaseomyces glabratus CBS 138
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19002
9 Samples
Download data: WIG
Series
Accession:
GSE59839
ID:
200059839
16.

RNA-Seq analysis of Candida glabrata wild-type and Cgset4Δ mutant in the presence and absence of the cell wall targeting echinocandin antifungal drug, caspofungin.

(Submitter supplied) To determine the effect of caspofungin (CSP) treatment and/or loss of the SET domain-containing CgSet4 protein on the transcriptional response of log-phase C. glabrata cells. RNA-Seq analysis was conducted on CAA medium-grown log-phase Candida glabrata wild-type (wt) and CgSET4-deleted (Cgset4D) cells in the presence and absence of caspofungin.
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL25492
8 Samples
Download data: XLSX
Series
Accession:
GSE202654
ID:
200202654
17.

Effect of depletion of ATP3 and ATP22 on gene expression of C. glabrata

(Submitter supplied) To uncover the underlying mechanism of fluconazole resistance upon genetic depletion of ATP3 and ATP22, we performed transcriptomic analysis by RNA-seq for atp3Δ, atp22Δ, and WT cells during standard log phase growth.
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL33385
10 Samples
Download data: TXT
Series
Accession:
GSE231872
ID:
200231872
18.

Inhibiting Fungal Multidrug Resistance by Disrupting an Activator-Mediator Interaction With the Small Molecule iKIX1

(Submitter supplied) Eukaryotic transcription activators stimulate the expression of specific sets of target genes through recruitment of co-activators such as the RNA polymerase II-interacting Mediator complex. We previously identified an activator-targeted ~85 amino acid three-helix bundle KIX domain in the human MED15 Mediator subunit that is structurally conserved in Gal11 Mediator subunits in fungi. The Gal11 KIX domain is engaged by pleiotropic drug resistance transcription factor (Pdr1) orthologues, key regulators of the multidrug resistance (MDR) pathway in S. more...
Organism:
Nakaseomyces glabratus; Saccharomyces cerevisiae
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17342 GPL21066
24 Samples
Download data: TXT
Series
Accession:
GSE74361
ID:
200074361
19.

Transcriptional profiling of putative J protein Jjj1 in Candida glabrata

(Submitter supplied) In the present study the gene encoding the putative J protein Jjj1 was deleted in a susceptible dose dependent clinical isolate resulting in decreased susceptibility to fluconazole compared to wild type. When JJJ1 was deleted in combination with the transcription factor PDR1 the fluconazole susceptibility was consistently only one fold higher from the strain deleted for PDR1 alone. Expression profiling was conducted to determine which genes have altered expression in the absence of JJJ1 and which of these alterations are dependent on PDR1 expression.
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24070
6 Samples
Download data: TXT, XLSX
Series
Accession:
GSE104476
ID:
200104476
20.

Histone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata

(Submitter supplied) This study explored the transcriptional change of Candida glabrata cells due to GCN5 deletion. We also compared the transcriptional responses to fluconazole and micafungin in WT and gcndelta cells relative to respective no drug controls.
Organism:
Nakaseomyces glabratus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL30061
12 Samples
Download data: TXT
Series
Accession:
GSE194310
ID:
200194310
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