fluconazole  (LKT Laboratories)

 
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  • 93
    Name:
    Fluconazole
    Description:
    Triazole 14 α demethylase inhibitor
    Catalog Number:
    f4682
    Price:
    45.3
    Purity:
    ≥98%
    Size:
    500 mg
    Category:
    Microbiology
    Buy from Supplier


    Structured Review

    LKT Laboratories fluconazole
    Structures of the triazoles voriconazole, <t>fluconazole</t> and itraconazole and the BR biosynthesis inhibitor Brz2001.
    Triazole 14 α demethylase inhibitor
    https://www.bioz.com/result/fluconazole/product/LKT Laboratories
    Average 93 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    fluconazole - by Bioz Stars, 2020-09
    93/100 stars

    Images

    1) Product Images from "Genetic Variation in Plant CYP51s Confers Resistance against Voriconazole, a Novel Inhibitor of Brassinosteroid-Dependent Sterol Biosynthesis"

    Article Title: Genetic Variation in Plant CYP51s Confers Resistance against Voriconazole, a Novel Inhibitor of Brassinosteroid-Dependent Sterol Biosynthesis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0053650

    Structures of the triazoles voriconazole, fluconazole and itraconazole and the BR biosynthesis inhibitor Brz2001.
    Figure Legend Snippet: Structures of the triazoles voriconazole, fluconazole and itraconazole and the BR biosynthesis inhibitor Brz2001.

    Techniques Used:

    Voriconazole, itraconazole and fluconazole induce phenotypes indicative of BR deficiency in arabidopsis and cress. ( A ) Arabidopsis plants grown on plates containing 5 µM of the indicated compounds under long-day conditions for 7 days. ( B ) Hypocotyl length of cress seedlings grown for 3 days on plates containing different concentrations of the indicated compounds. Data are the mean ± SD of 30 seedlings measured.
    Figure Legend Snippet: Voriconazole, itraconazole and fluconazole induce phenotypes indicative of BR deficiency in arabidopsis and cress. ( A ) Arabidopsis plants grown on plates containing 5 µM of the indicated compounds under long-day conditions for 7 days. ( B ) Hypocotyl length of cress seedlings grown for 3 days on plates containing different concentrations of the indicated compounds. Data are the mean ± SD of 30 seedlings measured.

    Techniques Used:

    2) Product Images from "Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance"

    Article Title: Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance

    Journal: Nature Communications

    doi: 10.1038/ncomms11128

    Msh2 alterations identified in diverse clinical isolates cause a mutator phenotype and increased emergence of antifungal resistance. ( a ) The 357 clinical isolates obtained were classified according to their susceptibilities to fluconazole (FLC) and the echinocandins (ECH), and the percentage of isolates within each group demonstrating a nonsynonymous msh2 mutation were determined. P value was determined through χ 2 analysis (compared with susceptible group). ( b ) All isolates were categorized by institution. Isolates demonstrating an msh2 mutation/total isolates are shown for each susceptibility group. See Supplementary Data 1 for a list of all individual isolates analyzed. ( c ) Echinocandin- (caspofungin) resistant colony frequencies of various clinical isolates were measured. ( d ) Wild type or msh2Δ cells expressing an empty or MSH2 -containing plasmid were selected on caspofungin and 5-fluoroanthranilic acid. See Supplementary Table 4 for strains. Frequency data in c , d are mean±s.d. from three independent experiments; representative images are shown. * P
    Figure Legend Snippet: Msh2 alterations identified in diverse clinical isolates cause a mutator phenotype and increased emergence of antifungal resistance. ( a ) The 357 clinical isolates obtained were classified according to their susceptibilities to fluconazole (FLC) and the echinocandins (ECH), and the percentage of isolates within each group demonstrating a nonsynonymous msh2 mutation were determined. P value was determined through χ 2 analysis (compared with susceptible group). ( b ) All isolates were categorized by institution. Isolates demonstrating an msh2 mutation/total isolates are shown for each susceptibility group. See Supplementary Data 1 for a list of all individual isolates analyzed. ( c ) Echinocandin- (caspofungin) resistant colony frequencies of various clinical isolates were measured. ( d ) Wild type or msh2Δ cells expressing an empty or MSH2 -containing plasmid were selected on caspofungin and 5-fluoroanthranilic acid. See Supplementary Table 4 for strains. Frequency data in c , d are mean±s.d. from three independent experiments; representative images are shown. * P

    Techniques Used: Mutagenesis, Expressing, Plasmid Preparation

    Deletion of MSH2 in C. glabrata leads to significantly more resistant colonies upon selection on multiple antifungal drugs. Wild type, msh2Δ and rad50Δ strains were selected on media containing caspofungin (an echinocandin), fluconazole (a triazole) and amphotericin B (a polyene) at concentrations from 16- to 32-fold greater than wild type MICs as described in Methods section. The plots show means of resistant colony frequencies from ≥3 independent experiments±s.d. See Supplementary Fig. 1 for resistant frequencies to voriconazole (triazole) and micafungin (echinocandin). ** P
    Figure Legend Snippet: Deletion of MSH2 in C. glabrata leads to significantly more resistant colonies upon selection on multiple antifungal drugs. Wild type, msh2Δ and rad50Δ strains were selected on media containing caspofungin (an echinocandin), fluconazole (a triazole) and amphotericin B (a polyene) at concentrations from 16- to 32-fold greater than wild type MICs as described in Methods section. The plots show means of resistant colony frequencies from ≥3 independent experiments±s.d. See Supplementary Fig. 1 for resistant frequencies to voriconazole (triazole) and micafungin (echinocandin). ** P

    Techniques Used: Selection

    3) Product Images from "Repeated Vulvovaginal Fungal Infections Cause Persistent Pain in a Mouse Model of Vulvodynia"

    Article Title: Repeated Vulvovaginal Fungal Infections Cause Persistent Pain in a Mouse Model of Vulvodynia

    Journal: Science translational medicine

    doi: 10.1126/scitranslmed.3002613

    Development of vulvar mechanical allodynia in a subset of mice after a single, extended SC5314 infection. ( A ) Experimental time-line illustrating the experimental procedures. An inoculation of 5 × 10 4 SC5314 cells was given on day 0; fluconazole
    Figure Legend Snippet: Development of vulvar mechanical allodynia in a subset of mice after a single, extended SC5314 infection. ( A ) Experimental time-line illustrating the experimental procedures. An inoculation of 5 × 10 4 SC5314 cells was given on day 0; fluconazole

    Techniques Used: Mouse Assay, Infection

    4) Product Images from "UPC2A Is Required for High-Level Azole Antifungal Resistance in Candida glabrata"

    Article Title: UPC2A Is Required for High-Level Azole Antifungal Resistance in Candida glabrata

    Journal: Antimicrobial Agents and Chemotherapy

    doi: 10.1128/AAC.02217-13

    Enhanced activity of fluconazole in an SDD clinical isolate, SM1, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest concentration
    Figure Legend Snippet: Enhanced activity of fluconazole in an SDD clinical isolate, SM1, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest concentration

    Techniques Used: Activity Assay, Concentration Assay

    Effect of UPC2A disruption on constitutive and fluconazole-induced gene expression. RNA was isolated from mid-log-phase cultures of parent clinical isolates, Δ upc2A mutants, and revertants, and qRT-PCR analysis of relative gene expression was
    Figure Legend Snippet: Effect of UPC2A disruption on constitutive and fluconazole-induced gene expression. RNA was isolated from mid-log-phase cultures of parent clinical isolates, Δ upc2A mutants, and revertants, and qRT-PCR analysis of relative gene expression was

    Techniques Used: Expressing, Isolation, Quantitative RT-PCR

    Enhanced activity of fluconazole in a resistant clinical isolate, SM3, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest
    Figure Legend Snippet: Enhanced activity of fluconazole in a resistant clinical isolate, SM3, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest

    Techniques Used: Activity Assay

    5) Product Images from "VT-1598 inhibits the in vitro growth of mucosal Candida strains and protects against fluconazole-susceptible and -resistant oral candidiasis in IL-17 signalling-deficient mice"

    Article Title: VT-1598 inhibits the in vitro growth of mucosal Candida strains and protects against fluconazole-susceptible and -resistant oral candidiasis in IL-17 signalling-deficient mice

    Journal: Journal of Antimicrobial Chemotherapy

    doi: 10.1093/jac/dky170

    VT-1598 provides remarkable protection against oral candidiasis in IL-17 signalling-deficient mice. (a–d) Act1 −/− mice were infected with C. albicans and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection. At day 5 post-infection, 24 h after the last drug dose, plasma (a) and tongue (b) drug concentrations were determined after infection with the fluconazole-susceptible C. albicans isolate Y72. Tongue cfu were determined in Act1 −/− mice infected with Y72 (c) or the fluconazole-resistant C. albicans isolate Y37 (d) at day 5 post-infection. (e) Tongue cfu were determined at day 5 post-infection from Act1 −/− mice infected with the fluconazole-susceptible C. albicans isolate Y72 and given VT-1598 or fluconazole starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection, but with 3.2 or 8 mg/kg dosing. (f) Act1 −/− mice were infected with Y72 and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 post-infection. Ten days after the last dose (day 14 post-infection), tongue fungal load was determined. Data were combined from 2–4 independent experiments with a total of 4–13 mice per group. Data were analysed using Mann–Whitney U -tests or unpaired t -tests, where appropriate. *, **, *** and **** indicate that the groups differ at P
    Figure Legend Snippet: VT-1598 provides remarkable protection against oral candidiasis in IL-17 signalling-deficient mice. (a–d) Act1 −/− mice were infected with C. albicans and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection. At day 5 post-infection, 24 h after the last drug dose, plasma (a) and tongue (b) drug concentrations were determined after infection with the fluconazole-susceptible C. albicans isolate Y72. Tongue cfu were determined in Act1 −/− mice infected with Y72 (c) or the fluconazole-resistant C. albicans isolate Y37 (d) at day 5 post-infection. (e) Tongue cfu were determined at day 5 post-infection from Act1 −/− mice infected with the fluconazole-susceptible C. albicans isolate Y72 and given VT-1598 or fluconazole starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection, but with 3.2 or 8 mg/kg dosing. (f) Act1 −/− mice were infected with Y72 and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 post-infection. Ten days after the last dose (day 14 post-infection), tongue fungal load was determined. Data were combined from 2–4 independent experiments with a total of 4–13 mice per group. Data were analysed using Mann–Whitney U -tests or unpaired t -tests, where appropriate. *, **, *** and **** indicate that the groups differ at P

    Techniques Used: Mouse Assay, Infection, MANN-WHITNEY

    6) Product Images from "Requirement for Ergosterol in V-ATPase Function Underlies Antifungal Activity of Azole Drugs"

    Article Title: Requirement for Ergosterol in V-ATPase Function Underlies Antifungal Activity of Azole Drugs

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1000939

    Synergy between fluconazole and amiodarone. (A) Early log phase cells expressing pHluorin were grown for 6 hours to mid log phase (OD ∼1) in SC minus leucine medium with or without fluconazole. Amiodarone (10 µM) was injected at the arrow . Measurement was done in triplicate, and the means and standard deviations are plotted [32] . (B) Early log phase WT cells expressing aequorin were grown with or without fluconazole for 4 hours. Amiodarone (10 µM) was injected at the arrow . Ca 2+ -dependent Aequorin luminescence was measured in triplicate as previously described [15] . For 45 Ca uptake, early log phase WT cells of S. cerevisiae (C) and C. albicans (D) were grown with or without fluconazole (20 µg/ml for S. cerevisiae , 1 µg/ml for C. albicans ) for 6 hours. Vacuolar vesicles isolated from these cultures were assayed for MgATP-dependent 45 CaCl 2 uptake as described in Materials and Methods [33] . Concanamycin A was added to assess V-ATPase dependence of CaCl 2 uptake. p values of two-tailed t-test were shown. (E) Mice infected with C. albicans (ATCC 36082) were treated with vehicle, fluconazole, amiodarone, and their combination intraperitoneally. On day 4 post-infection, mouse kidneys (5 per group) were removed, weighed, homogenized, serially diluted and then plated onto YPD agar plates containing chloramphenicol and ampicillin. CFU were counted after 48 hours. Means of CFU per gram of kidney under each treatment and standard errors are plotted.
    Figure Legend Snippet: Synergy between fluconazole and amiodarone. (A) Early log phase cells expressing pHluorin were grown for 6 hours to mid log phase (OD ∼1) in SC minus leucine medium with or without fluconazole. Amiodarone (10 µM) was injected at the arrow . Measurement was done in triplicate, and the means and standard deviations are plotted [32] . (B) Early log phase WT cells expressing aequorin were grown with or without fluconazole for 4 hours. Amiodarone (10 µM) was injected at the arrow . Ca 2+ -dependent Aequorin luminescence was measured in triplicate as previously described [15] . For 45 Ca uptake, early log phase WT cells of S. cerevisiae (C) and C. albicans (D) were grown with or without fluconazole (20 µg/ml for S. cerevisiae , 1 µg/ml for C. albicans ) for 6 hours. Vacuolar vesicles isolated from these cultures were assayed for MgATP-dependent 45 CaCl 2 uptake as described in Materials and Methods [33] . Concanamycin A was added to assess V-ATPase dependence of CaCl 2 uptake. p values of two-tailed t-test were shown. (E) Mice infected with C. albicans (ATCC 36082) were treated with vehicle, fluconazole, amiodarone, and their combination intraperitoneally. On day 4 post-infection, mouse kidneys (5 per group) were removed, weighed, homogenized, serially diluted and then plated onto YPD agar plates containing chloramphenicol and ampicillin. CFU were counted after 48 hours. Means of CFU per gram of kidney under each treatment and standard errors are plotted.

    Techniques Used: Expressing, Injection, Isolation, Two Tailed Test, Mouse Assay, Infection

    Fluconazole treatment disrupts V-ATPase function. (A) Vacuolar pH of WT (BY4742) cultures treated with fluconazole at specified concentrations for 6 hours in YPD. (B) Proton pumping rate and ATPase activity of WT (BY4742) cultures treated with or without fluconazole for 6 hours in YPD. Three independent batches of vacuolar vesicles were isolated and used to assay V-ATPase function. Cultures of upc2-1 mutant, WYP361, were treated with fluconazole (100 µg/ml), ergosterol (50 µM) or their combination at OD 0.1. Growth (C, representative of three independent experiments) was assessed at 8 hour post-treatment, and vacuolar pH (D) was assessed at 6 hour post-treatment. (E) WT C. albicans cells (SC5314) were grown in YPD with or without fluconazole for 5 hours. FM4-64 was added to the cultures to stain vacuoles for 30 min. Cells were chased with fresh YPD with or without fluconazole for 20 min followed by quinacrine addition for another 5 min. Fluorescence microscopic images of the cells were taken immediately after washing. Means and standard deviations are plotted. p values of two-tailed t-test are shown.
    Figure Legend Snippet: Fluconazole treatment disrupts V-ATPase function. (A) Vacuolar pH of WT (BY4742) cultures treated with fluconazole at specified concentrations for 6 hours in YPD. (B) Proton pumping rate and ATPase activity of WT (BY4742) cultures treated with or without fluconazole for 6 hours in YPD. Three independent batches of vacuolar vesicles were isolated and used to assay V-ATPase function. Cultures of upc2-1 mutant, WYP361, were treated with fluconazole (100 µg/ml), ergosterol (50 µM) or their combination at OD 0.1. Growth (C, representative of three independent experiments) was assessed at 8 hour post-treatment, and vacuolar pH (D) was assessed at 6 hour post-treatment. (E) WT C. albicans cells (SC5314) were grown in YPD with or without fluconazole for 5 hours. FM4-64 was added to the cultures to stain vacuoles for 30 min. Cells were chased with fresh YPD with or without fluconazole for 20 min followed by quinacrine addition for another 5 min. Fluorescence microscopic images of the cells were taken immediately after washing. Means and standard deviations are plotted. p values of two-tailed t-test are shown.

    Techniques Used: Activity Assay, Isolation, Mutagenesis, Staining, Fluorescence, Two Tailed Test

    7) Product Images from "Construction and Use of a Recyclable Marker To Examine the Role of Major Facilitator Superfamily Protein Members in Candida glabrata Drug Resistance Phenotypes"

    Article Title: Construction and Use of a Recyclable Marker To Examine the Role of Major Facilitator Superfamily Protein Members in Candida glabrata Drug Resistance Phenotypes

    Journal: mSphere

    doi: 10.1128/mSphere.00099-18

    Construction of a cdr1 Δ:: loxP allele using the new recyclable marker cassette. (A) Diagram showing the plasmid construct containing the cdr1 Δ:: loxP allele that was introduced into CBS138 cells with selection for nourseothricin resistance ( nat R ). This allele removes the entire CDR1 open reading frame (ORF). The result of recombination between the two loxP repeats is indicated by the arrow resolving to a single repeat denoted by the small black box. (B) Phenotypes of primary disruption mutants and evicted counterparts. Isogenic wild-type (CBS138), primary disruptants ( cdr1 Δ:: nat R ), and evicted disruptants ( cdr1 Δ:: loxP ) were grown to mid-log phase, and then serial dilutions were spotted across the plates. Two independent isolates of each disruptant were tested. (C) Complementation of the fluconazole-hypersensitive phenotype of the cdr1 Δ:: loxP allele by a plasmid-borne copy of CDR1 . Wild-type and cdr1 Δ:: loxP cells were transformed with an empty vector containing the nourseothricin resistance gene and served as controls for this experiment. The cdr1 Δ:: loxP cells were also transformed with the same vector plasmid containing a wild-type version of the CDR1 gene. The indicated transformants were serially diluted on rich YPD medium lacking or containing 5 μg/ml fluconazole (as well as 50 μg/ml nourseothricin to select for plasmid maintenance).
    Figure Legend Snippet: Construction of a cdr1 Δ:: loxP allele using the new recyclable marker cassette. (A) Diagram showing the plasmid construct containing the cdr1 Δ:: loxP allele that was introduced into CBS138 cells with selection for nourseothricin resistance ( nat R ). This allele removes the entire CDR1 open reading frame (ORF). The result of recombination between the two loxP repeats is indicated by the arrow resolving to a single repeat denoted by the small black box. (B) Phenotypes of primary disruption mutants and evicted counterparts. Isogenic wild-type (CBS138), primary disruptants ( cdr1 Δ:: nat R ), and evicted disruptants ( cdr1 Δ:: loxP ) were grown to mid-log phase, and then serial dilutions were spotted across the plates. Two independent isolates of each disruptant were tested. (C) Complementation of the fluconazole-hypersensitive phenotype of the cdr1 Δ:: loxP allele by a plasmid-borne copy of CDR1 . Wild-type and cdr1 Δ:: loxP cells were transformed with an empty vector containing the nourseothricin resistance gene and served as controls for this experiment. The cdr1 Δ:: loxP cells were also transformed with the same vector plasmid containing a wild-type version of the CDR1 gene. The indicated transformants were serially diluted on rich YPD medium lacking or containing 5 μg/ml fluconazole (as well as 50 μg/ml nourseothricin to select for plasmid maintenance).

    Techniques Used: Marker, Plasmid Preparation, Construct, Selection, Transformation Assay

    Phenotype profiling of isogenic CBS138 aqr1 , flr1 , and qdr2 deletion mutants. Serial dilutions of the indicated isogenic derivatives of CBS138 (wild type [wt]) were placed on these various media. All drugs were added to YPD at the following concentrations: 5 µg/ml fluconazole, 0.2 µg/ml itraconazole, 0.2 µg/ml ketoconazole, 2 µg/ml miconazole, 20 µg/ml terbinafine, and 3 mM diamide.
    Figure Legend Snippet: Phenotype profiling of isogenic CBS138 aqr1 , flr1 , and qdr2 deletion mutants. Serial dilutions of the indicated isogenic derivatives of CBS138 (wild type [wt]) were placed on these various media. All drugs were added to YPD at the following concentrations: 5 µg/ml fluconazole, 0.2 µg/ml itraconazole, 0.2 µg/ml ketoconazole, 2 µg/ml miconazole, 20 µg/ml terbinafine, and 3 mM diamide.

    Techniques Used:

    Interaction of Yap1- and Pdr1/Cdr1-regulated resistance pathways. (A) TDH3-YAP1 drives elevated diamide resistance independent of PDR1 or CDR1 . Isogenic wild-type, pdr1 Δ:: loxP , and cdr1 Δ:: loxP strains containing or lacking the TDH3-YAP1 allele were grown to mid-log phase and then serially diluted on plates containing the indicated concentrations of diamide. (B) The indicated strains were grown to mid-log phase and then serially diluted on rich medium containing 5 μg/ml fluconazole (FLC). (C) Complementation of fluconazole sensitivity in a cdr1 Δ flr1 Δ double mutant strain. Isogenic wild-type or cdr1 Δ flr1 Δ mutant strains were transformed with the plasmids indicated at left, which are all low-copy-number CEN-containing vectors with nourseothricin resistance. Both plates contain low-level nourseothricin (50 μg/ml) to ensure retention of the plasmids. (D) Diagram of interactions relating Pdr1/Cdr1 to Yap1/Flr1 and azole resistance. Arrows indicate positive interactions.
    Figure Legend Snippet: Interaction of Yap1- and Pdr1/Cdr1-regulated resistance pathways. (A) TDH3-YAP1 drives elevated diamide resistance independent of PDR1 or CDR1 . Isogenic wild-type, pdr1 Δ:: loxP , and cdr1 Δ:: loxP strains containing or lacking the TDH3-YAP1 allele were grown to mid-log phase and then serially diluted on plates containing the indicated concentrations of diamide. (B) The indicated strains were grown to mid-log phase and then serially diluted on rich medium containing 5 μg/ml fluconazole (FLC). (C) Complementation of fluconazole sensitivity in a cdr1 Δ flr1 Δ double mutant strain. Isogenic wild-type or cdr1 Δ flr1 Δ mutant strains were transformed with the plasmids indicated at left, which are all low-copy-number CEN-containing vectors with nourseothricin resistance. Both plates contain low-level nourseothricin (50 μg/ml) to ensure retention of the plasmids. (D) Diagram of interactions relating Pdr1/Cdr1 to Yap1/Flr1 and azole resistance. Arrows indicate positive interactions.

    Techniques Used: Mutagenesis, Transformation Assay, Low Copy Number

    8) Product Images from "Construction and Use of a Recyclable Marker To Examine the Role of Major Facilitator Superfamily Protein Members in Candida glabrata Drug Resistance Phenotypes"

    Article Title: Construction and Use of a Recyclable Marker To Examine the Role of Major Facilitator Superfamily Protein Members in Candida glabrata Drug Resistance Phenotypes

    Journal: mSphere

    doi: 10.1128/mSphere.00099-18

    Phenotype profiling of isogenic CBS138 aqr1 , flr1 , and qdr2 deletion mutants. Serial dilutions of the indicated isogenic derivatives of CBS138 (wild type [wt]) were placed on these various media. All drugs were added to YPD at the following concentrations: 5 µg/ml fluconazole, 0.2 µg/ml itraconazole, 0.2 µg/ml ketoconazole, 2 µg/ml miconazole, 20 µg/ml terbinafine, and 3 mM diamide.
    Figure Legend Snippet: Phenotype profiling of isogenic CBS138 aqr1 , flr1 , and qdr2 deletion mutants. Serial dilutions of the indicated isogenic derivatives of CBS138 (wild type [wt]) were placed on these various media. All drugs were added to YPD at the following concentrations: 5 µg/ml fluconazole, 0.2 µg/ml itraconazole, 0.2 µg/ml ketoconazole, 2 µg/ml miconazole, 20 µg/ml terbinafine, and 3 mM diamide.

    Techniques Used:

    Interaction of Yap1- and Pdr1/Cdr1-regulated resistance pathways. (A) TDH3-YAP1 drives elevated diamide resistance independent of PDR1 or CDR1 . Isogenic wild-type, pdr1 Δ:: loxP , and cdr1 Δ:: loxP strains containing or lacking the TDH3-YAP1 allele were grown to mid-log phase and then serially diluted on plates containing the indicated concentrations of diamide. (B) The indicated strains were grown to mid-log phase and then serially diluted on rich medium containing 5 μg/ml fluconazole (FLC). (C) Complementation of fluconazole sensitivity in a cdr1 Δ flr1 Δ double mutant strain. Isogenic wild-type or cdr1 Δ flr1 Δ mutant strains were transformed with the plasmids indicated at left, which are all low-copy-number CEN-containing vectors with nourseothricin resistance. Both plates contain low-level nourseothricin (50 μg/ml) to ensure retention of the plasmids. (D) Diagram of interactions relating Pdr1/Cdr1 to Yap1/Flr1 and azole resistance. Arrows indicate positive interactions.
    Figure Legend Snippet: Interaction of Yap1- and Pdr1/Cdr1-regulated resistance pathways. (A) TDH3-YAP1 drives elevated diamide resistance independent of PDR1 or CDR1 . Isogenic wild-type, pdr1 Δ:: loxP , and cdr1 Δ:: loxP strains containing or lacking the TDH3-YAP1 allele were grown to mid-log phase and then serially diluted on plates containing the indicated concentrations of diamide. (B) The indicated strains were grown to mid-log phase and then serially diluted on rich medium containing 5 μg/ml fluconazole (FLC). (C) Complementation of fluconazole sensitivity in a cdr1 Δ flr1 Δ double mutant strain. Isogenic wild-type or cdr1 Δ flr1 Δ mutant strains were transformed with the plasmids indicated at left, which are all low-copy-number CEN-containing vectors with nourseothricin resistance. Both plates contain low-level nourseothricin (50 μg/ml) to ensure retention of the plasmids. (D) Diagram of interactions relating Pdr1/Cdr1 to Yap1/Flr1 and azole resistance. Arrows indicate positive interactions.

    Techniques Used: Mutagenesis, Transformation Assay, Low Copy Number

    9) Product Images from "VT-1598 inhibits the in vitro growth of mucosal Candida strains and protects against fluconazole-susceptible and -resistant oral candidiasis in IL-17 signalling-deficient mice"

    Article Title: VT-1598 inhibits the in vitro growth of mucosal Candida strains and protects against fluconazole-susceptible and -resistant oral candidiasis in IL-17 signalling-deficient mice

    Journal: Journal of Antimicrobial Chemotherapy

    doi: 10.1093/jac/dky170

    VT-1598 provides remarkable protection against oral candidiasis in IL-17 signalling-deficient mice. (a–d) Act1 −/− mice were infected with C. albicans and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection. At day 5 post-infection, 24 h after the last drug dose, plasma (a) and tongue (b) drug concentrations were determined after infection with the fluconazole-susceptible C. albicans isolate Y72. Tongue cfu were determined in Act1 −/− mice infected with Y72 (c) or the fluconazole-resistant C. albicans isolate Y37 (d) at day 5 post-infection. (e) Tongue cfu were determined at day 5 post-infection from Act1 −/− mice infected with the fluconazole-susceptible C. albicans isolate Y72 and given VT-1598 or fluconazole starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection, but with 3.2 or 8 mg/kg dosing. (f) Act1 −/− mice were infected with Y72 and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 post-infection. Ten days after the last dose (day 14 post-infection), tongue fungal load was determined. Data were combined from 2–4 independent experiments with a total of 4–13 mice per group. Data were analysed using Mann–Whitney U -tests or unpaired t -tests, where appropriate. *, **, *** and **** indicate that the groups differ at P 
    Figure Legend Snippet: VT-1598 provides remarkable protection against oral candidiasis in IL-17 signalling-deficient mice. (a–d) Act1 −/− mice were infected with C. albicans and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection. At day 5 post-infection, 24 h after the last drug dose, plasma (a) and tongue (b) drug concentrations were determined after infection with the fluconazole-susceptible C. albicans isolate Y72. Tongue cfu were determined in Act1 −/− mice infected with Y72 (c) or the fluconazole-resistant C. albicans isolate Y37 (d) at day 5 post-infection. (e) Tongue cfu were determined at day 5 post-infection from Act1 −/− mice infected with the fluconazole-susceptible C. albicans isolate Y72 and given VT-1598 or fluconazole starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 days post-infection, but with 3.2 or 8 mg/kg dosing. (f) Act1 −/− mice were infected with Y72 and treated with vehicle, fluconazole (25 mg/kg) or VT-1598 (20 mg/kg) starting at 18 h post-infection and continued every 24 h thereafter at days 2, 3 and 4 post-infection. Ten days after the last dose (day 14 post-infection), tongue fungal load was determined. Data were combined from 2–4 independent experiments with a total of 4–13 mice per group. Data were analysed using Mann–Whitney U -tests or unpaired t -tests, where appropriate. *, **, *** and **** indicate that the groups differ at P 

    Techniques Used: Mouse Assay, Infection

    10) Product Images from "Horizontal Transmission of Candida albicans and Evidence of a Vaccine Response in Mice Colonized with the Fungus"

    Article Title: Horizontal Transmission of Candida albicans and Evidence of a Vaccine Response in Mice Colonized with the Fungus

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0022030

    Confirmation of horizontal transmission of C. albicans in mice treated with antibacterial agents. Antimicrobial-treated mice not fed C. albicans (groups B, D and H) housed in a common room (Panel A) with other groups of mice intentionally colonized with the fungus (+Ca), began showing evidence of fungal colonization by day 38 (group H) or after day 52 (groups B and D). Duplicate groups of B, D and H kept in an isolated room (i.e., groups B', D' and H', respectively) did not show evidence of the fungus in their feces (Panel B). p = penicillin; s = streptomycin; f = fluconazole; +Ca = C. albicans in drinking water on days 5–9; +Fba = vaccinated with Fba starting on day 31. The various symbols on the curves represent each animal subject.
    Figure Legend Snippet: Confirmation of horizontal transmission of C. albicans in mice treated with antibacterial agents. Antimicrobial-treated mice not fed C. albicans (groups B, D and H) housed in a common room (Panel A) with other groups of mice intentionally colonized with the fungus (+Ca), began showing evidence of fungal colonization by day 38 (group H) or after day 52 (groups B and D). Duplicate groups of B, D and H kept in an isolated room (i.e., groups B', D' and H', respectively) did not show evidence of the fungus in their feces (Panel B). p = penicillin; s = streptomycin; f = fluconazole; +Ca = C. albicans in drinking water on days 5–9; +Fba = vaccinated with Fba starting on day 31. The various symbols on the curves represent each animal subject.

    Techniques Used: Transmission Assay, Mouse Assay, Isolation

    Antibacterial therapy is required for a protracted GI-tract colonization with C. albicans . Mice received oral administration of various combinations of antimicrobial agents, live C. albicans, and a peptide (Fba) vaccine. Control groups did not receive one or more of the treatments. All groups that received at least two of the antibacterial agents and were fed C. albicans for a five day period (e.g., groups A, C and G) developed a protracted GI-tract colonization with the fungus as evidenced by the presence of the fungus in fecal specimens. Antibiotics were required for the fungal colonization as shown by the presence of C. albicans in the feces of group E only during the five day feeding period. Surprisingly, antibiotic-treated mice that were not fed C. albicans also became colonized (groups B, D and H). These results suggested the possibility that antibiotic-treated mice are susceptible to horizontal transmission of the fungus. p = penicillin; s = streptomycin; f = fluconazole; +Ca = C. albicans in drinking water on days 5–9; +Vac = vaccinated with Fba. Each mouse in each group is represented by an open circle, closed circle or closed triangle.
    Figure Legend Snippet: Antibacterial therapy is required for a protracted GI-tract colonization with C. albicans . Mice received oral administration of various combinations of antimicrobial agents, live C. albicans, and a peptide (Fba) vaccine. Control groups did not receive one or more of the treatments. All groups that received at least two of the antibacterial agents and were fed C. albicans for a five day period (e.g., groups A, C and G) developed a protracted GI-tract colonization with the fungus as evidenced by the presence of the fungus in fecal specimens. Antibiotics were required for the fungal colonization as shown by the presence of C. albicans in the feces of group E only during the five day feeding period. Surprisingly, antibiotic-treated mice that were not fed C. albicans also became colonized (groups B, D and H). These results suggested the possibility that antibiotic-treated mice are susceptible to horizontal transmission of the fungus. p = penicillin; s = streptomycin; f = fluconazole; +Ca = C. albicans in drinking water on days 5–9; +Vac = vaccinated with Fba. Each mouse in each group is represented by an open circle, closed circle or closed triangle.

    Techniques Used: Mouse Assay, Transmission Assay

    Body mass, GI-tract colonization and appearance of Candida albicans- specific antibodies as a function of time. Mice were given antibiotics in their water prior to and during ingestion of live C.albicans. Changes in body weight were monitored throughout the experiment, as was C. albicans colonization as measured by fungal colony forming units (CFU) per gram weight of feces (Panel A). One group was immunosuppressed (group 2) and all were followed for serum anti-mannan antibody induced as a result of GI-tract colonization. All mice were immunized and appearance of serum antibody against the vaccine immunogen, Fba, indicated whether they responded to the vaccine (Panel B, compare day 11 before vaccination to day 87 after vaccination). Groups 1 and 2 received antibacterial agents and fluconazole, but only group 2 was treated with cyclophosphamide. Group 3 was similar to 1, except that 3 did not receive fluconazole. Group 4 was not pretreated with antimicrobial agents prior to ingesting C. albicans, and this group was not maintained on gentamicin. Antibody responses were measured by ELISA for a 1∶100 dilution of each serum and are expressed as OD 490nm. Shown are antibody responses at days 11, 43 and 65 to a mannan fraction (α-mannan), which occurred as a result of GI-tract colonization, and antibody against Fba peptide, which occurred as a result of Fba vaccination (Panel B). In this experiment all mice were vaccinated on day 51 and boosted on days 65 and 79.
    Figure Legend Snippet: Body mass, GI-tract colonization and appearance of Candida albicans- specific antibodies as a function of time. Mice were given antibiotics in their water prior to and during ingestion of live C.albicans. Changes in body weight were monitored throughout the experiment, as was C. albicans colonization as measured by fungal colony forming units (CFU) per gram weight of feces (Panel A). One group was immunosuppressed (group 2) and all were followed for serum anti-mannan antibody induced as a result of GI-tract colonization. All mice were immunized and appearance of serum antibody against the vaccine immunogen, Fba, indicated whether they responded to the vaccine (Panel B, compare day 11 before vaccination to day 87 after vaccination). Groups 1 and 2 received antibacterial agents and fluconazole, but only group 2 was treated with cyclophosphamide. Group 3 was similar to 1, except that 3 did not receive fluconazole. Group 4 was not pretreated with antimicrobial agents prior to ingesting C. albicans, and this group was not maintained on gentamicin. Antibody responses were measured by ELISA for a 1∶100 dilution of each serum and are expressed as OD 490nm. Shown are antibody responses at days 11, 43 and 65 to a mannan fraction (α-mannan), which occurred as a result of GI-tract colonization, and antibody against Fba peptide, which occurred as a result of Fba vaccination (Panel B). In this experiment all mice were vaccinated on day 51 and boosted on days 65 and 79.

    Techniques Used: Mouse Assay, Enzyme-linked Immunosorbent Assay

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    Injection:

    Article Title: Mechanism of the Synergistic Effect of Amiodarone and Fluconazole in Candida albicans ▿ ▿ †
    Article Snippet: .. At 3 h postinfection, mice were given single or in combination treatments of AMD (Amiodarone-HCl injection; Bioniche) and FLC (LKT Laboratories, Inc.) via the intraperitoneal route. .. AMD treatment doses ranged between 5.0 to 25 mg/kg, while FLC doses ranged from 0.1 to 1 mg/kg in mice infected with FLC-susceptible strains and from 5.0 to 40 mg/kg for animals infected with FLC-resistant strains.

    other:

    Article Title: Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance
    Article Snippet: Fluconazole (LKT Laboratories, Saint Paul, MN), caspofungin (Merck, Rahway, NJ) and micafungin (Astellas, Deerfield, IL) were dissolved and diluted according to CLSI standards .

    Article Title: Genetic Variation in Plant CYP51s Confers Resistance against Voriconazole, a Novel Inhibitor of Brassinosteroid-Dependent Sterol Biosynthesis
    Article Snippet: Chemicals Bifonazole, fluconazole, itraconazole, thiabendazole and uniconazole were purchased from LKT Laboratories (St. Paul, MN, USA).

    Mouse Assay:

    Article Title: Requirement for Ergosterol in V-ATPase Function Underlies Antifungal Activity of Azole Drugs
    Article Snippet: .. Mice were treated with vehicle, Fluconazole (LKT Laboratories Inc., St. Paul, MN) (0.1 to 60 mg/kg of body weight/dose), Amiodarone (Henry Schein Animal Health, Melville, NY) (5.0 or 25 mg/kg of body weight/dose) or Fluconazole (0.1 to 60 mg/kg of body weight/dose) + Amiodarone (5.0 or 25 mg/kg of body weight/dose) administered intraperitoneally once a day for a total of 4 days. .. On day 4 post-infection, kidneys from euthanized mice (5 per group, unless specified) were aseptically removed, weighed, and homogenized in sterile saline using an IKA Works ULTRA TURRAX Tube Disperser Workstation (IKA Works Inc., Wilmington, NC).

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    Article Title: Mechanism of the Synergistic Effect of Amiodarone and Fluconazole in Candida albicans ▿ ▿ †
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    LKT Laboratories fluconazole
    Structures of the triazoles voriconazole, <t>fluconazole</t> and itraconazole and the BR biosynthesis inhibitor Brz2001.
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    Structures of the triazoles voriconazole, fluconazole and itraconazole and the BR biosynthesis inhibitor Brz2001.

    Journal: PLoS ONE

    Article Title: Genetic Variation in Plant CYP51s Confers Resistance against Voriconazole, a Novel Inhibitor of Brassinosteroid-Dependent Sterol Biosynthesis

    doi: 10.1371/journal.pone.0053650

    Figure Lengend Snippet: Structures of the triazoles voriconazole, fluconazole and itraconazole and the BR biosynthesis inhibitor Brz2001.

    Article Snippet: Chemicals Bifonazole, fluconazole, itraconazole, thiabendazole and uniconazole were purchased from LKT Laboratories (St. Paul, MN, USA).

    Techniques:

    Voriconazole, itraconazole and fluconazole induce phenotypes indicative of BR deficiency in arabidopsis and cress. ( A ) Arabidopsis plants grown on plates containing 5 µM of the indicated compounds under long-day conditions for 7 days. ( B ) Hypocotyl length of cress seedlings grown for 3 days on plates containing different concentrations of the indicated compounds. Data are the mean ± SD of 30 seedlings measured.

    Journal: PLoS ONE

    Article Title: Genetic Variation in Plant CYP51s Confers Resistance against Voriconazole, a Novel Inhibitor of Brassinosteroid-Dependent Sterol Biosynthesis

    doi: 10.1371/journal.pone.0053650

    Figure Lengend Snippet: Voriconazole, itraconazole and fluconazole induce phenotypes indicative of BR deficiency in arabidopsis and cress. ( A ) Arabidopsis plants grown on plates containing 5 µM of the indicated compounds under long-day conditions for 7 days. ( B ) Hypocotyl length of cress seedlings grown for 3 days on plates containing different concentrations of the indicated compounds. Data are the mean ± SD of 30 seedlings measured.

    Article Snippet: Chemicals Bifonazole, fluconazole, itraconazole, thiabendazole and uniconazole were purchased from LKT Laboratories (St. Paul, MN, USA).

    Techniques:

    Msh2 alterations identified in diverse clinical isolates cause a mutator phenotype and increased emergence of antifungal resistance. ( a ) The 357 clinical isolates obtained were classified according to their susceptibilities to fluconazole (FLC) and the echinocandins (ECH), and the percentage of isolates within each group demonstrating a nonsynonymous msh2 mutation were determined. P value was determined through χ 2 analysis (compared with susceptible group). ( b ) All isolates were categorized by institution. Isolates demonstrating an msh2 mutation/total isolates are shown for each susceptibility group. See Supplementary Data 1 for a list of all individual isolates analyzed. ( c ) Echinocandin- (caspofungin) resistant colony frequencies of various clinical isolates were measured. ( d ) Wild type or msh2Δ cells expressing an empty or MSH2 -containing plasmid were selected on caspofungin and 5-fluoroanthranilic acid. See Supplementary Table 4 for strains. Frequency data in c , d are mean±s.d. from three independent experiments; representative images are shown. * P

    Journal: Nature Communications

    Article Title: Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance

    doi: 10.1038/ncomms11128

    Figure Lengend Snippet: Msh2 alterations identified in diverse clinical isolates cause a mutator phenotype and increased emergence of antifungal resistance. ( a ) The 357 clinical isolates obtained were classified according to their susceptibilities to fluconazole (FLC) and the echinocandins (ECH), and the percentage of isolates within each group demonstrating a nonsynonymous msh2 mutation were determined. P value was determined through χ 2 analysis (compared with susceptible group). ( b ) All isolates were categorized by institution. Isolates demonstrating an msh2 mutation/total isolates are shown for each susceptibility group. See Supplementary Data 1 for a list of all individual isolates analyzed. ( c ) Echinocandin- (caspofungin) resistant colony frequencies of various clinical isolates were measured. ( d ) Wild type or msh2Δ cells expressing an empty or MSH2 -containing plasmid were selected on caspofungin and 5-fluoroanthranilic acid. See Supplementary Table 4 for strains. Frequency data in c , d are mean±s.d. from three independent experiments; representative images are shown. * P

    Article Snippet: Fluconazole (LKT Laboratories, Saint Paul, MN), caspofungin (Merck, Rahway, NJ) and micafungin (Astellas, Deerfield, IL) were dissolved and diluted according to CLSI standards .

    Techniques: Mutagenesis, Expressing, Plasmid Preparation

    Deletion of MSH2 in C. glabrata leads to significantly more resistant colonies upon selection on multiple antifungal drugs. Wild type, msh2Δ and rad50Δ strains were selected on media containing caspofungin (an echinocandin), fluconazole (a triazole) and amphotericin B (a polyene) at concentrations from 16- to 32-fold greater than wild type MICs as described in Methods section. The plots show means of resistant colony frequencies from ≥3 independent experiments±s.d. See Supplementary Fig. 1 for resistant frequencies to voriconazole (triazole) and micafungin (echinocandin). ** P

    Journal: Nature Communications

    Article Title: Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance

    doi: 10.1038/ncomms11128

    Figure Lengend Snippet: Deletion of MSH2 in C. glabrata leads to significantly more resistant colonies upon selection on multiple antifungal drugs. Wild type, msh2Δ and rad50Δ strains were selected on media containing caspofungin (an echinocandin), fluconazole (a triazole) and amphotericin B (a polyene) at concentrations from 16- to 32-fold greater than wild type MICs as described in Methods section. The plots show means of resistant colony frequencies from ≥3 independent experiments±s.d. See Supplementary Fig. 1 for resistant frequencies to voriconazole (triazole) and micafungin (echinocandin). ** P

    Article Snippet: Fluconazole (LKT Laboratories, Saint Paul, MN), caspofungin (Merck, Rahway, NJ) and micafungin (Astellas, Deerfield, IL) were dissolved and diluted according to CLSI standards .

    Techniques: Selection

    Development of vulvar mechanical allodynia in a subset of mice after a single, extended SC5314 infection. ( A ) Experimental time-line illustrating the experimental procedures. An inoculation of 5 × 10 4 SC5314 cells was given on day 0; fluconazole

    Journal: Science translational medicine

    Article Title: Repeated Vulvovaginal Fungal Infections Cause Persistent Pain in a Mouse Model of Vulvodynia

    doi: 10.1126/scitranslmed.3002613

    Figure Lengend Snippet: Development of vulvar mechanical allodynia in a subset of mice after a single, extended SC5314 infection. ( A ) Experimental time-line illustrating the experimental procedures. An inoculation of 5 × 10 4 SC5314 cells was given on day 0; fluconazole

    Article Snippet: Mice in both the SC5314-infected and the control groups were treated with fluconazole (15 mg/kg, once daily for 7 days; LKT Laboratories) administered via oral gavage.

    Techniques: Mouse Assay, Infection

    Enhanced activity of fluconazole in an SDD clinical isolate, SM1, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest concentration

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: UPC2A Is Required for High-Level Azole Antifungal Resistance in Candida glabrata

    doi: 10.1128/AAC.02217-13

    Figure Lengend Snippet: Enhanced activity of fluconazole in an SDD clinical isolate, SM1, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest concentration

    Article Snippet: Antifungal agents were obtained from the following sources: fluconazole was from LKT Laboratories (St. Paul, MN), miconazole was from MP Biomedicals, Inc. (Solon, OH), anidulafungin and voriconazole were from Pfizer (New York, NY), and ketoconazole, amphotericin B, lovastatin, and terbinafine were from Sigma (St. Louis, MO).

    Techniques: Activity Assay, Concentration Assay

    Effect of UPC2A disruption on constitutive and fluconazole-induced gene expression. RNA was isolated from mid-log-phase cultures of parent clinical isolates, Δ upc2A mutants, and revertants, and qRT-PCR analysis of relative gene expression was

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: UPC2A Is Required for High-Level Azole Antifungal Resistance in Candida glabrata

    doi: 10.1128/AAC.02217-13

    Figure Lengend Snippet: Effect of UPC2A disruption on constitutive and fluconazole-induced gene expression. RNA was isolated from mid-log-phase cultures of parent clinical isolates, Δ upc2A mutants, and revertants, and qRT-PCR analysis of relative gene expression was

    Article Snippet: Antifungal agents were obtained from the following sources: fluconazole was from LKT Laboratories (St. Paul, MN), miconazole was from MP Biomedicals, Inc. (Solon, OH), anidulafungin and voriconazole were from Pfizer (New York, NY), and ketoconazole, amphotericin B, lovastatin, and terbinafine were from Sigma (St. Louis, MO).

    Techniques: Expressing, Isolation, Quantitative RT-PCR

    Enhanced activity of fluconazole in a resistant clinical isolate, SM3, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: UPC2A Is Required for High-Level Azole Antifungal Resistance in Candida glabrata

    doi: 10.1128/AAC.02217-13

    Figure Lengend Snippet: Enhanced activity of fluconazole in a resistant clinical isolate, SM3, with a disruption of UPC2A . (A) Minimum fungicidal concentrations were determined by spotting cultures on solid media after 48 h of growth in liquid RPMI medium. The MFC is the lowest

    Article Snippet: Antifungal agents were obtained from the following sources: fluconazole was from LKT Laboratories (St. Paul, MN), miconazole was from MP Biomedicals, Inc. (Solon, OH), anidulafungin and voriconazole were from Pfizer (New York, NY), and ketoconazole, amphotericin B, lovastatin, and terbinafine were from Sigma (St. Louis, MO).

    Techniques: Activity Assay