Transcriptional profiling of azole-resistant Candida parapsilosis strains
Open accessAbstract
Herein we describe the changes in the gene expression profile of Candida parapsilosis associated with the acquisition of experimentally induced resistance to azole antifungal drugs. Three resistant strains of C. parapsilosis were obtained following prolonged in vitro exposure of a susceptible clinical isolate to constant concentrations of fluconazole, voriconazole, or posaconazole. We found that after incubation with fluconazole or voriconazole, strains became resistant to both azoles but not to posaconazole, although susceptibility to this azole decreased, whereas the strain incubated with posaconazole displayed resistance to the three azoles. The resistant strains obtained after exposure to fluconazole and to voriconazole have increased expression of the transcription factor MRR1, the major facilitator transporter MDR1, and several reductases and oxidoreductases. Interestingly, and similarly to what has been described in C. albicans, upregulation of MRR1 and MDR1 is correlated with point mutations in MRR1 in the resistant strains. The resistant strain obtained after exposure to posaconazole shows upregulation of two transcription factors (UPC2 and NDT80) and increased expression of 13 genes involved in ergosterol biosynthesis. This is the first study addressing global molecular mechanisms underlying azole resistance in C. parapsilosis; the results suggest that similarly to C. albicans, tolerance to azoles involves the activation of efflux pumps and/or increased ergosterol synthesis.
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Written from the paper’s full text.
TL;DR
This study generated three azole-resistant Candida parapsilosis strains in vitro and used microarray profiling to show that fluconazole/voriconazole resistance involves MRR1/MDR1 efflux upregulation, while posaconazole resistance involves UPC2/NDT80 and ergosterol biosynthesis genes. It is described as the first study addressing global molecular mechanisms underlying azole resistance in C. parapsilosis.
Key findings
- After 60 days of exposure to fluconazole (16 μg/ml), voriconazole (2 μg/ml), or posaconazole (1 μg/ml), resistant strains BC014RFLC and BC014RVRC had MICs of 128 μg/ml FLC, 4 μg/ml VRC, and 0.5 μg/ml PSC; BC014RPSC had MICs of 128 μg/ml FLC, 16 μg/ml VRC, and 32 μg/ml PSC. Resistance was stable after 60 days without drug, with no MIC decrease greater than 1 dilution.
- Microarray analysis found differential expression (FC > 2, P < 0.05) of 1,128 genes (595 upregulated, 533 downregulated) in BC014RFLC, 210 genes (138 upregulated, 72 downregulated) in BC014RVRC, and 598 genes (341 upregulated, 257 downregulated) in BC014RPSC.
- BC014RFLC and BC014RVRC shared 130 differentially regulated genes, representing 62% of total genes in BC014RVRC; these included increased expression of MRR1, MDR1, and several reductases/oxidoreductases. MDR1 was upregulated 19.43-fold in BC014RFLC and 40.22-fold in BC014RVRC, but unchanged in BC014RPSC; MRR1 upregulation correlated with point mutations in MRR1.
- BC014RPSC showed upregulation of transcription factors UPC2 and NDT80 and increased expression of 13 genes involved in ergosterol biosynthesis; GO analysis found sterol biosynthesis overrepresented (19/409 cluster frequency vs 32/5,085 background, corrected P = 1.17E−10).
Methods
- A single azole-susceptible clinical isolate, C. parapsilosis BC014S, was subcultured daily for 60 days in RPMI 1640 with constant fluconazole, voriconazole, or posaconazole, generating BC014RFLC, BC014RVRC, and BC014RPSC. MICs were determined by CLSI M27-A3/M27-S3, with population analysis and stability testing after 60 days without antifungal drug.
- RNA from overnight YEPD cultures without antifungal drugs was profiled on Agilent C. parapsilosis microarrays (GPL13192) covering 5,834 putative ORFs, with four biological replicates per experiment including two dye swaps. Data were analyzed with Limma, Loess normalization, and thresholds of FC > 2 and adjusted P < 0.05; selected genes were confirmed by RT-qPCR, and MRR1, UPC2, and NDT80 were sequenced. Raw data are in GEO accession GSE27409.
Limitations
- The paper does not include a dedicated limitations section.
- Evident from the text: resistance was induced in vitro from a single susceptible clinical isolate (BC014S), so findings may not represent clinical azole-resistant C. parapsilosis populations or in vivo resistance development.
- Evident from the text: transcriptome profiling was performed on strains grown without antifungal drugs, measuring constitutive changes rather than acute drug exposure; one posaconazole array failed quality control and was discarded as an outlier.
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- Findingown data§ RESULTS AND DISCUSSION
In BC014RPSC, GO terms associated with sterol biosynthesis, response to chemical synthesis, and response to drugs are overrepresented.
“whereas in the BC014RPSC strain, GO terms associated with sterol biosynthesis, response to chemical synthesis, and response to drugs are overrepresented”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
- Findingown data§ RESULTS AND DISCUSSION
Population analysis demonstrated the homogeneous nature of the population for all three resistant strains, excluding the possibility that a mixture of susceptible and resistant clones was present in the final cultures.
“Population analysis clearly demonstrated the homogeneous nature of the population for all strains (data not shown), excluding the possibility that a mixture of susceptible and resistant clones is present in the final cultures.”
Quote in the paperSubstantial claim - Findingown data§ RESULTS AND DISCUSSION
In BC014RVRC, the GO term associated with response to chemical stimulus is overrepresented.
“In BC014RVRC, the GO term associated with response to chemical stimulus is overrepresented”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
- Findingown data§ Abstract
Upregulation of MRR1 and MDR1 is correlated with point mutations in MRR1 in the resistant strains.
“Interestingly, and similarly to what has been described in C. albicans, upregulation of MRR1 and MDR1 is correlated with point mutations in MRR1 in the resistant strains.”
Quote in the paperSubstantial claim - Findingown data§ Abstract
Three resistant C. parapsilosis strains were obtained after prolonged in vitro exposure of a susceptible clinical isolate to constant concentrations of fluconazole, voriconazole, or posaconazole.
“Three resistant strains of C. parapsilosis were obtained following prolonged in vitro exposure of a susceptible clinical isolate to constant concentrations of fluconazole, voriconazole, or posaconazole.”
- Also stated in: § MATERIALS AND METHODS · plain
“In summary, three resistant strains were generated from the initial susceptible strain, strain BC014S, which were designated BC014RFLC, BC014RVRC, and BC014RPSC.”
Quote in the paperSubstantial claim - Also stated in: § MATERIALS AND METHODS · plain
- Findingown data§ RESULTS AND DISCUSSION
Cluster 2 contains MDR1 and CPAG_03790, both members of the major facilitator superfamily (MFS) of multidrug transporters.
“Cluster 2 contains MDR1 and CPAG_03790 genes, both members of the major facilitator superfamily (MFS) of multidrug transporters.”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
- Findingown data§ Abstract
The strain obtained after exposure to posaconazole developed resistance to all three azoles (fluconazole, voriconazole, and posaconazole) with high MIC values.
“whereas the strain incubated with posaconazole displayed resistance to the three azoles.”
- Also stated in: § RESULTS AND DISCUSSION · plain
“In addition, the strain obtained after exposure to posaconazole (BC014RPSC) developed resistance to all three azoles, with high MIC values.”
Quote in the paperSubstantial claim - Also stated in: § RESULTS AND DISCUSSION · plain
- Findingown data§ RESULTS AND DISCUSSION
Expression of a third member of the MFS family (CPAG_01932) was also increased, albeit to a lesser extent.
“Expression of a third member of the MFS family (CPAG_01932) was also increased, albeit to a lesser extent (cluster 1; Fig. 3; Table 5).”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
- Premisecitation§ MATERIALS AND METHODS
The azole concentrations used (16 μg/ml fluconazole, 2 μg/ml voriconazole, and 1 μg/ml posaconazole) are similar to therapeutic blood levels achieved during antifungal therapy.
“These concentrations are similar to therapeutic blood levels achieved during antifungal therapy (8).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [8]
Not checked in the free run.
- May combine two claims. 15
- Classified as probably not a substantial claim. 14
May combine two claims.
Findingown data§ AbstractThe resistant strains obtained after exposure to fluconazole and voriconazole have increased expression of the transcription factor MRR1, the major facilitator transporter MDR1, and several reductases and oxidoreductases.
“The resistant strains obtained after exposure to fluconazole and to voriconazole have increased expression of the transcription factor MRR1, the major facilitator transporter MDR1, and several reductases and oxidoreductases.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ RESULTS AND DISCUSSIONAzoles impaired the expression of genes involved in multiple cellular processes, resulting in a pleiotropic effect upon gene expression.
“Azoles impaired the expression of genes involved in multiple cellular processes, resulting in a pleiotropic effect upon gene expression.”
Quote in the paperSubstantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
May combine two claims.
Findingown data§ AbstractThe resistant strain obtained after exposure to posaconazole shows upregulation of two transcription factors (UPC2 and NDT80) and increased expression of 13 genes involved in ergosterol biosynthesis.
“The resistant strain obtained after exposure to posaconazole shows upregulation of two transcription factors (UPC2 and NDT80) and increased expression of 13 genes involved in ergosterol biosynthesis.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ RESULTS AND DISCUSSIONExpression of MDR1 is upregulated by 19.43-fold in BC014RFLC and 40.22-fold in BC014RVRC, confirmed by RT-qPCR, whereas its expression in BC014RPSC remained unchanged.
“Expression of MDR1 is upregulated by 19.43- and 40.22-fold (confirmed by RT-qPCR; Fig. 4) in BC014RFLC and BC014RVRC strains, whereas its expression in the BC014RPSC strain remained unchanged.”
Quote in the paperSubstantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
May combine two claims.
Findingown data§ RESULTS AND DISCUSSIONClusters 1, 2, and 3 contain genes with increased expression in BC014RFLC and BC014RVRC strains; cluster 3 showed the greatest changes in gene expression.
“Clusters 1, 2, and 3 contain genes with increased expression in BC014RFLC and BC014RVRC strains; cluster 3 showed the greatest changes in gene expression”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
May combine two claims.
Findingown data§ AbstractThe strains obtained after exposure to fluconazole or voriconazole became resistant to both fluconazole and voriconazole but not to posaconazole, although susceptibility to posaconazole decreased (posaconazole MIC increased 4 dilutions).
“We found that after incubation with fluconazole or voriconazole, strains became resistant to both azoles but not to posaconazole, although susceptibility to this azole decreased”
- Also stated in: § RESULTS AND DISCUSSION · plain
“Strains obtained after exposure to either fluconazole (BC014RFLC) or voriconazole (BC014RVOR) acquired resistance to both drugs, but not to posaconazole, although the posaconazole MIC value increased 4 dilutions.”
Quote in the paperSubstantial claim- Also stated in: § RESULTS AND DISCUSSION · plain
May combine two claims.
Findingown data§ RESULTS AND DISCUSSIONAll three induced resistant strains maintained a stable resistance pattern after subculturing in the absence of antifungal drugs for 60 days, with no decrease greater than 1 dilution in MIC values.
“All three induced resistant strains maintained a stable resistance pattern after they were subcultured in the absence of antifungal drugs for 60 days. No decrease greater than 1 dilution was found in MIC values (data not shown).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown data§ RESULTS AND DISCUSSION130 genes were differentially regulated in both BC014RFLC and BC014RVRC, representing 62% of total genes in BC014RVRC.
“Because BC014RFLC and BC014RVRC strains displayed similar resistance profiles, the genes that were differentially regulated in both were identified (130 genes, representing 62% of total genes in BC014RVRC).”
Quote in the paperSubstantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
May combine two claims.
Findingown data§ RESULTS AND DISCUSSIONIn BC014RFLC, up to 13% of upregulated genes were associated with RNA metabolic processes and ribosome biogenesis and 10% were associated with translation.
“However, in the BC014RFLC strain, up to 13% of the upregulated genes were associated with RNA metabolic processes and ribosome biogenesis and 10% were associated with translation”
Quote in the paperNot a substantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
May combine two claims.
Findingown data§ RESULTS AND DISCUSSIONMicroarray analysis identified differential expression (FC > 2, P < 0.05) of 1,128 genes (595 upregulated and 533 downregulated) in BC014RFLC, 210 genes (138 upregulated and 72 downregulated) in BC014RVRC, and 598 genes (341 upregulated and 257 downregulated) in BC014RPSC.
“Microarray analysis identified differential expression (FC > 2, P < 0.05) of 1,128 (595 upregulated and 533 downregulated), 210 (138 upregulated and 72 downregulated), and 598 (341 upregulated and 257 downregulated) genes in BC014RFLC, BC014RVRC, and BC014RPSC strains, respectively”
Quote in the paperSubstantial claim- The authors state this as an assumption: Duplicate probes within each array can be considered technical replicates.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ INTRODUCTIONThe authors previously described the in vitro development of stable azole resistance in C. parapsilosis, which was induced rapidly following fluconazole exposure or more slowly when exposed to posaconazole.
“We previously described the in vitro development of stable azole resistance in C. parapsilosis, which was induced rapidly following fluconazole exposure or more slowly when it was exposed to posaconazole (PSC) (47).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [47]
Not checked in the free run.
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Premisecitation§ INTRODUCTIONPoint mutations in genes coding for the target enzyme, reducing azole target affinity, are a mechanism of azole resistance in Candida species.
“point mutations in genes coding for the target enzyme, reducing azole target affinity (61)”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [61]
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ INTRODUCTIONPrevious studies with C. albicans, C. dubliniensis, and C. tropicalis demonstrated that resistance to fluconazole can be promoted following repeated in vitro exposure to the drug.
“Previous studies with C. albicans (38), C. dubliniensis (59), and C. tropicalis (9) demonstrated that resistance to fluconazole can be promoted following repeated in vitro exposure to the drug.”
Quote in the paperNot a substantial claim0 of 3 sources checkedClassified as probably not a substantial claim.
Study design and conductnone given§ MATERIALS AND METHODSIn each microarray experiment, four biological replicates (including two dye swaps) were prepared.
“In each experiment, four biological replicates (including two dye swaps) were prepared.”
- Also stated in: § MATERIALS AND METHODS · plain
“In each experiment, four biological replicates were performed.”
Quote in the paperSubstantial claim- Also stated in: § MATERIALS AND METHODS · plain
May combine two claims.
Interpretationown data§ AbstractTolerance to azoles in C. parapsilosis, similarly to C. albicans, involves the activation of efflux pumps and/or increased ergosterol synthesis.
“the results suggest that similarly to C. albicans, tolerance to azoles involves the activation of efflux pumps and/or increased ergosterol synthesis.”
- Also stated in: § INTRODUCTION · hedged
“Our results suggest that, similar to C. albicans, C. parapsilosis acquires resistance to azoles either through upregulation of the MDR1 multidrug transporter family or via increased expression of the sterol biosynthetic pathway.”
Quote in the paperSubstantial claim- Also stated in: § INTRODUCTION · hedged
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ INTRODUCTIONIncreased production of the azole target enzyme is a mechanism of azole resistance in Candida species.
“increased production of the azole target enzyme (23, 27, 63)”
Quote in the paperNot a substantial claim0 of 3 sources checkedClassified as probably not a substantial claim.
Study design and conductnone given§ MATERIALS AND METHODSOnly RNA samples yielding 28S rRNA/18S rRNA ratios ranging from 1.6 to 2.2 and showing absence of degradation were used in subsequent analyses.
“Only samples yielding 28S rRNA/18S rRNA ratios ranging from 1.6 to 2.2 and showing the absence of degradation were used in subsequent analyses.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ INTRODUCTIONFailure to accumulate the drug intracellularly may be caused by lack of drug penetration due to changes in membrane lipids and sterols or by active efflux of drugs, particularly from overexpression of CDR1, CDR2, and MDR1.
“failure to accumulate the drug intracellularly, which may be caused by the lack of drug penetration, due to changes in membrane lipids and sterols (28), or by active efflux of drugs, resulting particularly from overexpression of the CDR1, CDR2, and MDR1 genes (3, 38, 62, 73)”
Quote in the paperNot a substantial claim0 of 5 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductcitation§ MATERIALS AND METHODSThe C. parapsilosis ATCC 22019 type strain was used for quality control of antifungal susceptibility testing.
“The C. parapsilosis ATCC 22019 type strain from the American Type Culture Collection was used for quality control of antifungal susceptibility testing, as recommended (15, 16).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [15]
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- cites [16]
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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductcitation§ MATERIALS AND METHODSQuality controls were performed to assess the good quality of the arrays and to verify the presence of any chromosomal bias expression.
“Quality controls were performed in order to assess the good quality of the arrays and to verify the presence of any chromosomal bias expression (7) (data not shown).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [7]
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Classified as probably not a substantial claim.
Study design and conductnone given§ MATERIALS AND METHODSOnly probes with a fold change greater than 2 and an adjusted P value less than 0.05 were used in analyses.
“Only probes with a fold change (FC) of greater than 2 and an adjusted P value of less than 0.05 were used in analyses.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown data§ MATERIALS AND METHODSRaw microarray data and the description of the array were deposited in the Gene Expression Omnibus Database under accession number GSE27409.
“Raw microarray data and the description of the array have been deposited in the Gene Expression Omnibus Database under accession number GSE27409 (superseries).”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductcitation§ MATERIALS AND METHODSMIC values of fluconazole, voriconazole, and posaconazole were determined according to the CLSI M27-A3 protocol and M27-S3 supplement.
“MIC values of FLC, VRC, and PSC were determined according to the M27-A3 protocol and the M27-S3 supplement of the Clinical and Laboratory Standards Institute (CLSI) (15, 16).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [15]
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- cites [16]
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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone given§ MATERIALS AND METHODSFor each RT-qPCR, five replicates for each strain were integrated, and the signal obtained for each gene was normalized with the TUB4 signal.
“For each real-time quantitative PCR (RT-qPCR), five replicates for each strain were integrated.”
- Also stated in: § MATERIALS AND METHODS · plain
“The signal obtained for each gene was normalized with the TUB4 signal.”
Quote in the paperNot a substantial claim- Also stated in: § MATERIALS AND METHODS · plain
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown data§ MATERIALS AND METHODSOne array in the posaconazole experiment did not pass quality control and was discarded as an outlier.
“One of the arrays in the posaconazole experiment did not pass our quality control and it was therefore discarded as an outlier.”
Quote in the paperNot a substantial claim
The paper relies on this without support.
There are scarce data regarding mechanisms of azole resistance in C. parapsilosis.
“However, there are still scarce data regarding mechanisms of azole resistance in C. parapsilosis.”
The authors state this as an assumption.
Duplicate probes within each array can be considered technical replicates.
“Duplicate probes within each array were considered technical replicates. This assumption allows full advantage of the platform design to be taken by analyzing the within-array replicate spots using a pooled correlation method.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Resistance to azoles in C. parapsilosis has been attributed to mutations in MRR1 and ERG11 (Y132F alone or with R398I), and overexpression of CDR1, MDR1, and ERG11.
“Resistance to azoles in C. parapsilosis has been attributed to mutations in the transcription factor gene MRR1 [84] and ERG11 (Y132F, either alone or in combination with an R398I) [85,86,87], and overexpression of CDR1, MDR1, and ERG11 [85,86,88].”
From Evolutionary Emergence of Drug Resistance in Candida Opportunistic Pathogens (2018) · cites this paper as [88]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Voriconazole-resistant strain has two identifiers
MinorThe results call the strain obtained after voriconazole exposure BC014RVOR, whereas the methods identify that strain as BC014RVRC.
“Strains obtained after exposure to either fluconazole (BC014RFLC) or voriconazole (BC014RVOR) acquired resistance to both drugs”
“three resistant strains were generated from the initial susceptible strain, strain BC014S, which were designated BC014RFLC, BC014RVRC, and BC014RPSC.”
Cites
MUSCLE: multiple sequence alignment with high accuracy and high throughput
Edgar, R. C. (2004) · Nucleic Acids Research · doi:10.1093/nar/gkh340 · Cited by 44,662 · see citing works
Epidemiology of Invasive Candidiasis: a Persistent Public Health Problem
Pfaller, M. A., & Diekema, D. J. (2007) · Clinical Microbiology Reviews · doi:10.1128/cmr.00029-06 · Cited by 4,174 · cited 2× · see citing works
“Candida parapsilosis is the second most common Candida species isolated from patients with bloodstream infections in Latin America and Asia (46, 60), and it is also commonly found in European surveys (4, 17, 43, 67).”
BackgroundHoffman, C. S., & Winston, F. (1987) · Gene · doi:10.1016/0378-1119(87)90131-4 · Cited by 2,492 · see citing works
Normalization of cDNA microarray data
Smyth, G. K., & Speed, T. (2003) · Methods · doi:10.1016/s1046-2023(03)00155-5 · Cited by 1,871 · see citing works
Evolution of pathogenicity and sexual reproduction in eight Candida genomes
Butler, G., Rasmussen, M. D., Lin, M. F., Santos, M. A. S., Sakthikumar, S., Munro, C. A., Rheinbay, E., Grabherr, M., Forche, A., Reedy, J. L., et al. (2009) · Nature · doi:10.1038/nature08064 · Cited by 1,065 · see citing works
Self-citationWingard, J. R., Merz, W. G., Rinaldi, M. G., Johnson, T. R., Karp, J. E., & Saral, R. (1991) · New England Journal of Medicine · doi:10.1056/nejm199110313251803 · Cited by 937 · see citing works
Resistance of Candida species to antifungal agents: molecular mechanisms and clinical consequences
Sanglard, D., & Odds, F. C. (2002) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(02)00181-0 · Cited by 784 · see citing works
White, T. C. (1997) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.41.7.1482 · Cited by 612 · see citing works
Efflux-Mediated Antifungal Drug Resistance
Cannon, R. D., Lamping, E., Holmes, A. R., Niimi, K., Baret, P. V., Keniya, M. V., Tanabe, K., Niimi, M., Goffeau, A., & Monk, B. C. (2009) · Clinical Microbiology Reviews · doi:10.1128/cmr.00051-08 · Cited by 608 · see citing works
Sanglard, D., Ischer, F., Koymans, L. M. H., & Billé, J. (1998) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.42.2.241 · Cited by 465 · see citing works
Pfaller, M. A., & Diekema, D. J. (2004) · Clinical Microbiology and Infection · doi:10.1111/j.1470-9465.2004.t01-1-00844.x · Cited by 422 · see citing works
Coste, A. T., Karababa, M., Ischer, F., Bille, J., & Sanglard, D. (2004) · Eukaryotic Cell · doi:10.1128/ec.3.6.1639-1652.2004 · Cited by 407 · see citing works
Sanglard, D., Ischer, F., Monod, M., & Billé, J. (1996) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.40.10.2300 · Cited by 402 · see citing works
Pfaller, M. A., Boyken, L. B., Hollis, R. J., Kroeger, J. S., Messer, S. A., Tendolkar, S., & Diekema, D. J. (2007) · Journal of Clinical Microbiology · doi:10.1128/jcm.01901-07 · Cited by 389 · see citing works
Pfaller, M. A., Jones, R. N., Doern, G. V., Sader, H. S., Messer, S. A., Houston, A., Coffman, S., Hollis, R. J., & The SENTRY Participant Group (2000) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.44.3.747-751.2000 · Cited by 378 · see citing works
Morschhäuser, J., Barker, K. S., Liu, T. T., Blaß-Warmuth, J., Homayouni, R., & Rogers, P. D. (2007) · PLoS Pathogens · doi:10.1371/journal.ppat.0030164 · Cited by 355 · see citing works
Wingard, J. R., Merz, W. G., Rinaldi, M. G., Miller, C. B., Karp, J. E., & Saral, R. (1993) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.37.9.1847 · Cited by 339 · see citing works
A High-Affinity Iron Permease Essential for <i>Candida albicans</i> Virulence
Ramanan, N., & Wang, Y. (2000) · Science · doi:10.1126/science.288.5468.1062 · Cited by 336 · see citing works
Liu, T. T., Lee, R. E. B., Barker, K. S., Lee, R. E., Wei, L., Homayouni, R., & Rogers, P. D. (2005) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.49.6.2226-2236.2005 · Cited by 313 · see citing works
Regulation of multidrug resistance in pathogenic fungi
Morschhäuser, J. (2010) · Fungal Genetics and Biology · doi:10.1016/j.fgb.2009.08.002 · Cited by 300 · see citing works
Hwang, C., Rhie, G., Oh, J., Huh, W., Yim, H., & Kang, S.-O. (2002) · Microbiology · doi:10.1099/00221287-148-11-3705 · Cited by 293 · see citing works
An update on antifungal targets and mechanisms of resistance in<i>Candida</i><i>albicans</i>
Akins, R. A. (2005) · Medical Mycology · doi:10.1080/13693780500138971 · Cited by 291 · see citing works
Vermitsky, J.-P., & Edlind, T. D. (2004) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.48.10.3773-3781.2004 · Cited by 285 · see citing works
Dunkel, N., Blaß, J., Rogers, P. D., & Morschhäuser, J. (2008) · Molecular Microbiology · doi:10.1111/j.1365-2958.2008.06309.x · Cited by 278 · see citing works
Li, X., Madison, V., Chau, A. S., Loebenberg, D., Palermo, R. E., & McNicholas, P. M. (2004) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.48.2.568-574.2004 · Cited by 266 · see citing works
Multiple efflux mechanisms are involved in Candida albicans fluconazole resistance
Albertson, G. D., Niimi, M., Cannon, R. D., & Jenkinson, H. F. (1996) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.40.12.2835 · Cited by 260 · see citing works
Alarco, A., & Raymond, M. (1999) · Journal of Bacteriology · doi:10.1128/jb.181.3.700-708.1999 · Cited by 244 · see citing works
Almirante, B., Rodríguez-Pardo, D., Cuenca‐Estrella, M., Almela, M., Sánchez, F., Ayats, J., Alonso-Tarrés, C., Rodrı́guez-Tudela, J. L., Pahissa, A., & the Barcelona Candidemia Project Study Group (2006) · Journal of Clinical Microbiology · doi:10.1128/jcm.44.5.1681-1685.2006 · Cited by 241 · see citing works
Dunkel, N., Liu, T. T., Barker, K. S., Homayouni, R., Morschhäuser, J., & Rogers, P. D. (2008) · Eukaryotic Cell · doi:10.1128/ec.00103-08 · Cited by 236 · see citing works
De Backer, M. D., Ilyina, T., Ma, X.-J., Vandoninck, S., Luyten, W. H. M. L., & Vanden Bossche, H. (2001) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.45.6.1660-1670.2001 · Cited by 211 · see citing works
Mobilization of Intracellular Copper Stores by the Ctr2 Vacuolar Copper Transporter
Rees, E. M., Lee, J., & Thiele, D. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m411669200 · Cited by 207 · see citing works
Pre-processing Agilent microarray data
ZAHURAK, M. L., Parmigiani, G., Yu, W., Scharpf, R. B., Berman, D. M., Schaeffer, E. M., Shabbeer, S., & Cope, L. (2007) · BMC Bioinformatics · doi:10.1186/1471-2105-8-142 · Cited by 197 · see citing works
Diethylcarbamazine-related antimicrobial activity in Mycobacterium tuberculosis-infected blood
Kitchen, L. W. (1998) · Journal of Antimicrobial Chemotherapy · doi:10.1093/jac/42.2.241 · Cited by 183 · see citing works
Sarvikivi, E., Lyytikäinen, O., Soll, D. R., Pujol, C., Pfaller, M. A., Richardson, M. D., Koukila-Kähkölä, P., Luukkainen, P., & Saxén, H. (2005) · Journal of Clinical Microbiology · doi:10.1128/jcm.43.6.2729-2735.2005 · Cited by 177 · see citing works
Marr, K. A., Lyons, C. N., Rustad, T., Bowden, R. A., & White, T. C. (1998) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.42.10.2584 · Cited by 166 · see citing works
Candida parapsilosisCharacterization in an Outbreak Setting
Kuhn, D. M., Mukherjee, P. K., Clark, T. A., Pujol, C., Chandra, J., Hajjeh, R. A., Warnock, D. W., Soll, D. R., & Ghannoum, M. A. (2004) · Emerging infectious diseases · doi:10.3201/eid1006.030873 · Cited by 161 · see citing works
Karababa, M., Coste, A. T., Rognon, B., Billé, J., & Sanglard, D. (2004) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.48.8.3064-3079.2004 · Cited by 161 · see citing works
Rogers, P. D., & Barker, K. S. (2003) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.47.4.1220-1227.2003 · Cited by 157 · see citing works
van den Hazel, H. B., Pichler, H., Matta, M. A. D. V., Leitner, E., Goffeau, A., & Daum, G. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.4.1934 · Cited by 157 · see citing works
Sandven, P. (2000) · PubMed · Cited by 153 · see citing works
Prasad, T., Chandra, A., Mukhopadhyay, C. K., & Prasad, R. (2006) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.00653-06 · Cited by 149 · see citing works
Experimental Induction of Fluconazole Resistance in <i>Candida tropicalis</i> ATCC 750
Barchiesi, F., Calabrese, D., Sanglard, D., Falconi Di Francesco, L., Caselli, F., Giannini, D., Giacometti, A., Gavaudan, S., & Scalise, G. (2000) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.44.6.1578-1584.2000 · Cited by 145 · see citing works
Heilmann, C. J., Schneider, S., Barker, K. S., Rogers, P. D., & Morschhäuser, J. (2010) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01102-09 · Cited by 142 · see citing works
Role of aCandida albicansP1-Type ATPase in Resistance to Copper and Silver Ion Toxicity
Riggle, P. J., & Kumamoto, C. A. (2000) · Journal of Bacteriology · doi:10.1128/jb.182.17.4899-4905.2000 · Cited by 128 · see citing works
Silva, A. P., Miranda, I. M., Lisboa, C., Pina‐Vaz, C., & Rodrigues, A. G. (2009) · Journal of Clinical Microbiology · doi:10.1128/jcm.02379-08 · Cited by 122 · see citing works
Self-citationClustering Approaches to Identifying Gene Expression Patterns from DNA Microarray Data
Do, J. H., & Choi, D. (2008) · Molecules and Cells · doi:10.1016/s1016-8478(23)17582-0 · Cited by 121 · see citing works
Barker, K. S. (2004) · Journal of Antimicrobial Chemotherapy · doi:10.1093/jac/dkh336 · Cited by 117 · see citing works
Inducible Azole Resistance Associated with a Heterogeneous Phenotype in Candida albicans
Marr, K. A., Lyons, C. N., Ha, K. C., Rustad, T. R., & White, T. C. (2001) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.45.1.52-59.2001 · Cited by 106 · see citing works
Pfaller, M. A., Diekema, D. J., Gibbs, D. L., Newell, V. A., Ng, K. P., Colombo, A. L., Finquelievich, J. L., Barnes, R. A., & Wadula, J. (2008) · Journal of Clinical Microbiology · doi:10.1128/jcm.02122-07 · Cited by 105 · see citing works
The Lipid Composition of Azole-sensitive and Azole-resistant Strains of Candida albicans
Hitchcock, C. A., Barrett-Bee, K. J., & Russell, N. J. (1986) · Microbiology · doi:10.1099/00221287-132-9-2421 · Cited by 98 · see citing works
Antifungal therapy in invasive fungal infections
Chen, S. C. ‐., Playford, E. G., & Sorrell, T. C. (2010) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2010.06.002 · Cited by 98 · see citing works
The zinc cluster transcription factor Tac1p regulates PDR16 expression in Candida albicans
Znaidi, S., Deken, X. D., Weber, S., Rigby, T., Nantel, A., & Raymond, M. (2007) · Molecular Microbiology · doi:10.1111/j.1365-2958.2007.05931.x · Cited by 97 · see citing works
A first Portuguese epidemiological survey of fungaemia in a university hospital
Costa‐de‐Oliveira, S., Pina‐Vaz, C., Mendonça, D. M., & Rodrigues, A. G. (2008) · European Journal of Clinical Microbiology & Infectious Diseases · doi:10.1007/s10096-007-0448-4 · Cited by 97 · see citing works
Self-citationChanges in susceptibility to posaconazole in clinical isolates of Candida albicans
Li, X. (2003) · Journal of Antimicrobial Chemotherapy · doi:10.1093/jac/dkh027 · Cited by 96 · see citing works
Analysis of gene evolution and metabolic pathways using the Candida Gene Order Browser
Fitzpatrick, D. A., Gaora, P. Ó., Byrne, K. P., & Butler, G. (2010) · BMC Genomics · doi:10.1186/1471-2164-11-290 · Cited by 95 · see citing works
Self-citationCorrelation between Biofilm Formation and the Hypoxic Response in Candida parapsilosis
Rossignol, T., Ding, C., Guida, A., d’Enfert, C., Higgins, D. G., & Butler, G. (2009) · Eukaryotic Cell · doi:10.1128/ec.00350-08 · Cited by 92 · see citing works
Self-citationRole of Ndt80p in Sterol Metabolism Regulation and Azole Resistance in <i>Candida albicans</i>
Sellam, A., Tebbji, F., & Nantel, A. (2009) · Eukaryotic Cell · doi:10.1128/ec.00074-09 · Cited by 91 · see citing works
Andes, D. R., Forrest, A., Lepak, A. J., Nett, J. E., Marchillo, K., & Lincoln, L. (2006) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01053-05 · Cited by 76 · see citing works
Transcriptional Response of Candida parapsilosis following Exposure to Farnesol
Rossignol, T., Logue, M. E., Reynolds, K., Grenon, M., Lowndes, N. F., & Butler, G. (2007) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01438-06 · Cited by 75 · see citing works
Self-citationProtchenko, O. V., Rodriguez-Suarez, R. J., Androphy, R., Bussey, H., & Philpott, C. C. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m512812200 · Cited by 73 · see citing works
Schubert, S., Rogers, P. D., & Morschhäuser, J. (2008) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.00740-08 · Cited by 73 · see citing works
Significant differences in drug susceptibility among species in the Candida parapsilosis group
Asbeck, E. C. V., Clemons, K. V., Martinez, M., Tong, A.-J., & Stevens, D. A. (2008) · Diagnostic Microbiology and Infectious Disease · doi:10.1016/j.diagmicrobio.2008.04.019 · Cited by 70 · see citing works
Efflux Pumps in Drug Resistance of Candida
Prasad, R., Gaur, N., Gaur, M., & Komath, S. (2006) · Infectious Disorders - Drug Targets · doi:10.2174/187152606784112164 · Cited by 64 · see citing works
Ruhnke, M. (2000) · Journal of Antimicrobial Chemotherapy · doi:10.1093/jac/46.2.291 · Cited by 63 · see citing works
Hof, H. (2008) · Drug Resistance Updates · doi:10.1016/j.drup.2008.01.001 · Cited by 60 · see citing works
Riggle, P. J., & Kumamoto, C. A. (2006) · Eukaryotic Cell · doi:10.1128/ec.00243-06 · Cited by 56 · see citing works
Arbour, M., Epp, E., Hogues, H., Sellam, A., Lacroix, C., Rauceo, J. M., Mitchell, A. P., Whiteway, M. S., & Nantel, A. (2009) · FEMS Yeast Research · doi:10.1111/j.1567-1364.2009.00563.x · Cited by 55 · see citing works
Proteomic Analysis of Azole Resistance in Candida albicans Clinical Isolates
Hooshdaran, M. Z., Barker, K. S., Hilliard, G. M., Kusch, H., Morschhäuser, J., & Rogers, P. D. (2004) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.48.7.2733-2735.2004 · Cited by 55 · see citing works
Development of Candidemia on Caspofungin Therapy: a Case Report
Cheung, C. N., Guo, Y., Gialanella, P., & Feldmesser, M. (2006) · Infection · doi:10.1007/s15010-006-5613-7 · Cited by 53 · see citing works
Posteraro, B., Bruno, S., Boccia, S., et al. (2004) · Infection Control and Hospital Epidemiology · doi:10.1086/502454 · Cited by 51 · see citing works
Kusch, H., Biswas, K., Schwanfelder, S., Engelmann, S., Rogers, P. D., Hecker, M., & Morschhäuser, J. (2004) · Molecular Genetics and Genomics · doi:10.1007/s00438-004-0984-x · Cited by 44 · see citing works
Voriconazole and multidrug resistance in Candida albicans
Wakieć, R., Prasad, R., Morschhäuser, J., Barchiesi, F., Borowski, E., & Milewski, S. (2006) · Mycoses · doi:10.1111/j.1439-0507.2006.01327.x · Cited by 39 · see citing works
Andes, D. R., Lepak, A. J., Nett, J. E., Lincoln, L., & Marchillo, K. (2006) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01305-05 · Cited by 38 · see citing works
Dynamics ofin vitro acquisition of resistance byCandida parapsilosisto different azoles
Silva, A. P., Costa‐de‐Oliveira, S., Silva-Dias, A., Pina‐Vaz, C., & Rodrigues, A. G. (2009) · FEMS Yeast Research · doi:10.1111/j.1567-1364.2009.00508.x · Cited by 32 · see citing works
Self-citationDNA microarray analysis of fluconazole resistance in a laboratory Candida albicans strain
Yan, L., Zhang, J., Li, M., Cao, Y., Xu, Z. Q., Cao, Y., Gao, P., Wang, Y., & Jiang, Y. (2008) · Acta Biochimica et Biophysica Sinica · doi:10.1111/j.1745-7270.2008.00483.x · Cited by 31 · see citing works
Xu, Z. Q., Zhang, L., Zhang, J., Cao, Y., Yu, Y.-Y., Wang, D., Ying, K., Chen, W., & Jiang, Y. (2006) · International Journal of Medical Microbiology · doi:10.1016/j.ijmm.2006.03.004 · Cited by 30 · see citing works
Miguel, L. G. S., Plá, J., Cobo, J., Navarro, F., Sánchez-Sousa, A., Alvarez, M. E., Martos, I., & Moreno, S. (2004) · Diagnostic Microbiology and Infectious Disease · doi:10.1016/j.diagmicrobio.2004.03.017 · Cited by 28 · see citing works
de Repentigny, L., St‐Germain, G., Charest, H., et al. (2008) · The Pediatric Infectious Disease Journal · doi:10.1097/inf.0b013e3181634f2b · Cited by 26 · see citing works
Deken, X. D., & Raymond, M. (2004) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.48.7.2700-2703.2004 · Cited by 23 · see citing works
Perea, J. R. A., Garcia-Quetglas, E., & Sádaba, B. (2007) · Revista Iberoamericana de Micología · doi:10.1016/s1130-1406(07)70047-5 · Cited by 23 · see citing works
Flagged first, then by citations
Research works printed but not linked: 3
- AzanzaJ. R. Garcia-QuetglasE. SadabaB.. 2007. Pharmacology of azoles. Rev. Iberoam. Micol. 24:223–227.(In Spanish.)
- Clinical Laboratory Standards Institute 2008. Reference method for broth dilution antifungal susceptibility testing of yeasts, 3rd ed. Approved standard M27-A3. Clinical and Laboratory Standards Institute, Wayne, PA.
- Clinical Laboratory Standards Institute. 2008. Reference method for broth dilution antifungal susceptibility testing of yeasts. Third informational supplement: document M27-S3. Clinical and Laboratory Standards Institute, Wayne, PA.
Cited by
Sorted by citations
Azole Antifungal Resistance in Candida albicans and Emerging Non-albicans Candida Species
Whaley, S. G., Berkow, E. L., Rybak, J. M., Nishimoto, A. T., Barker, K. S., & Rogers, P. D. (2017) · Frontiers in Microbiology · doi:10.3389/fmicb.2016.02173 · Cited by 900 · see citing works
Mechanisms of <i>Candida</i> Biofilm Drug Resistance
Taff, H. T., Mitchell, K. F., Edward, J. A., & Andes, D. R. (2013) · Future Microbiology · doi:10.2217/fmb.13.101 · Cited by 422 · see citing works
Candida parapsilosis: from genes to the bedside
Tóth, R., Nosek, J., Mora-Montes, H. M., Gabaldon, T., Bliss, J. M., Nosanchuk, J. D., Turner, S. A., Butler, G., Vágvölgyi, C., & Gácser, A. (2019) · Clinical Microbiology Reviews · doi:10.1128/cmr.00111-18 · Cited by 327 · see citing works
Self-citationEmerging and Emerged Pathogenic Candida Species: Beyond the Candida albicans Paradigm
Papon, N., Courdavault, V., Clastre, M., & Bennett, R. J. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003550 · Cited by 314 · see citing works
Evolutionary Emergence of Drug Resistance in Candida Opportunistic Pathogens
Ksiezopolska, E., & Gabaldón, T. (2018) · Genes · doi:10.3390/genes9090461 · Cited by 230 · see citing works
Souza, A. C. R., Fuchs, B. B., Pinhati, H. M. S., Siqueira, R. A., Hagen, F., Meis, J. F., Mylonakis, E., & Colombo, A. L. (2015) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01177-15 · Cited by 121 · see citing works
Grossman, N. T., Pham, C. D., Cleveland, A. A., & Lockhart, S. R. (2015) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.04613-14 · Cited by 112 · see citing works
Espinel-Ingroff, A., Pfaller, M. A., Bustamante, B., Canton, E., Fothergill, A., Fuller, J., Gonzalez, G. M., Lass-Flörl, C., Lockhart, S. R., Martin-Mazuelos, E., et al. (2014) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.02615-13 · Cited by 105 · see citing works
Berkow, E. L., Manigaba, K., Parker, J. E., Barker, K. S., Kelly, S. L., & Rogers, P. D. (2015) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.01358-15 · Cited by 95 · see citing works
Zhang, L., Xiao, M., Watts, M. R., Wang, H., Fan, X., Kong, F., & Xu, Y.-C. (2015) · BMC Infectious Diseases · doi:10.1186/s12879-015-1086-6 · Cited by 62 · see citing works
Rybak, J. M., Dickens, C. M., Parker, J. E., Caudle, K. E., Manigaba, K., Whaley, S. G., Nishimoto, A. T., Luna-Tapia, A., Roy, S., Zhang, Q., et al. (2017) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.00651-17 · Cited by 53 · see citing works
Papp, C., Bohner, F., Kocsis, K., Varga, M., Szekeres, A., Bodai, L., Willis, J. R., Gabaldón, T., Tóth, R., Nosanchuk, J. D., et al. (2020) · mSphere · doi:10.1128/msphere.00821-20 · Cited by 42 · see citing works
Costa, C., Ribeiro, J., Miranda, I. M., Silva-Dias, A., Cavalheiro, M., Costa-de-Oliveira, S., Rodrigues, A. G., & Teixeira, M. C. (2016) · Frontiers in Microbiology · doi:10.3389/fmicb.2016.00526 · Cited by 43 · see citing works
Self-citationJoshua, I., & Höfken, T. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18040772 · Cited by 40 · see citing works
Zinc and Iron Homeostasis: Target-Based Drug Screening as New Route for Antifungal Drug Development
Simm, C., & May, R. C. (2019) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2019.00181 · Cited by 26 · see citing works
- Authors
- Silva, A. P., Miranda, I. M., Guida, A., Synnott, J., Rocha, R., Silva, R., Amorim, A., Pina-Vaz, C., Butler, G., & Rodrigues, A. G.
- Affiliations
- Universidade do Porto (PT)
- University College Dublin (IE)
- Department of Microbiology, Faculty of Medicine, University of Porto, Porto, Portugal
- Venue
- Antimicrobial Agents and Chemotherapy
- Publisher
- American Society for Microbiology
- Published
- 2011-07
- Volume
- 55
- Issue
- 7
- Pages
- 3546-3556
- ISSN
- 0066-4804 (ISSN-L)
- 1098-6596
- PMC
- PMC3122401
- OpenAlex
- W2115530382
- Semantic Scholar
- f1ca7462bac9a92d57f835b8f4fbd1400531ed26
- Cited by
- 86
- References
- 80
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 1 · 2023: 7 · 2022: 7 · 2021: 5 · 2020: 9 · 2019: 5 · 2018: 8 · 2017: 9 · 2016: 7 · 2015: 6 · 2014: 5 · 2013: 4 · 2012: 4
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antimicrobial Agents and Chemotherapy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Science Foundation Ireland
- University College Dublin
- Universidade do Porto
- Fundação para a Ciência e a Tecnologia
- European Social Fund
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
- Keywords
- Candida parapsilosis, azole resistance, fluconazole, voriconazole, posaconazole, gene expression profiling, MRR1, MDR1, efflux pumps, ergosterol biosynthesis, UPC2, Ndt80, antifungal resistance, transcription factor mutations
- MeSH terms
- Antifungal Agents, Azoles, Candida, Fungal Proteins, Microbial Sensitivity Tests, Pyrimidines, Triazoles, Fluconazole, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Drug Resistance, Fungal, Voriconazole
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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