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  • 99
    Millipore clotrimazole
    Activation of NF-κB antagonizes SXR signaling and inhibits expression of the SXR target gene CYP3A4. ( A ) HepG2 cells were transfected with SXR-dependent reporter (XREM-LUC) with control or SXR expression vectors. Cells were treated with 10 μM RIF in the presence or absence of TPA (0.1 μM). ( B ) p65 inhibits SXR transactivation and IκBαM rescues p65-mediated inhibition of SXR-dependent reporter gene activation. p65 or IκBαM was used at a 1:1 ratio with SXR expression vector. After transfection, cells were treated with 10 μM RIF, <t>clotrimazole,</t> or RU486 for 24 hours before the assay. ( C ) Human primary hepatocytes and ( D and E ) LS180 cells were treated for 24 hours with 10 μM RIF, clotrimazole, or RU486 in the presence or absence of 0.1 μM TPA or 10 ng/ml TNF-α, as indicated. ( F ) Mouse primary hepatocytes were treated for 24 hours with 10 μM PCN in the presence or absence of 10 ng/ml mouse TNF-α. Total RNAs were isolated, and expression of human CYP3A4 and SXR genes as well as mouse CYP3A11 gene was determined by QRT-PCR assays.
    Clotrimazole, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 641 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 641 article reviews
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    92
    Selleck Chemicals clotrimazole
    Activation of NF-κB antagonizes SXR signaling and inhibits expression of the SXR target gene CYP3A4. ( A ) HepG2 cells were transfected with SXR-dependent reporter (XREM-LUC) with control or SXR expression vectors. Cells were treated with 10 μM RIF in the presence or absence of TPA (0.1 μM). ( B ) p65 inhibits SXR transactivation and IκBαM rescues p65-mediated inhibition of SXR-dependent reporter gene activation. p65 or IκBαM was used at a 1:1 ratio with SXR expression vector. After transfection, cells were treated with 10 μM RIF, <t>clotrimazole,</t> or RU486 for 24 hours before the assay. ( C ) Human primary hepatocytes and ( D and E ) LS180 cells were treated for 24 hours with 10 μM RIF, clotrimazole, or RU486 in the presence or absence of 0.1 μM TPA or 10 ng/ml TNF-α, as indicated. ( F ) Mouse primary hepatocytes were treated for 24 hours with 10 μM PCN in the presence or absence of 10 ng/ml mouse TNF-α. Total RNAs were isolated, and expression of human CYP3A4 and SXR genes as well as mouse CYP3A11 gene was determined by QRT-PCR assays.
    Clotrimazole, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Tocris clotrimazole
    Effects of K Ca channel blockers on Gly‐Sar‐stimulated jejunal Isc response in mice. Inhibitory effect of TRAM‐34, <t>Clotrimazole,</t> lberiotoxin and Apamin on the time course of Gly‐Sar stimulated jejunal mucosal I sc (a–d). Gly‐Sar was added to mucosal side after TRAM‐34 (10 μM) Clotrimazole (30 μM), lberiotoxin (100 nM) or Apamin (100 nM) were added to different sides of the tissues for 20 min (e–h). (d, f and h) Summarize the data comparing the effects of Ca 2+ omission plus TRAM‐34, Clotrimazole, lberiotoxin and Apamin on Gly‐Sar‐induced ∆ I sc. Data are given as mean ± SEM ( n = 5 in each series), * p
    Clotrimazole, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    FUJIFILM clotrimazole
    NDSB cosolubilization relieves the artificial inhibition of enzymatic activity. The aggregation-prone compounds, I4PTH (0.2 m m ; ▪), <t>clotrimazole</t> (0.4 m m ; ▪), and benzyl benzoate (1.0 m m ; ▪), were added to the reaction solutions of the chymotrypsin assays with the indicated concentrations of NDSB256. The bars indicate the amount of product in the presence of the aggregation-prone compounds relative to that in the absence of the aggregation-prone compounds.
    Clotrimazole, supplied by FUJIFILM, used in various techniques. Bioz Stars score: 93/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Bayer AG clotrimazole
    <t>Clotrimazole</t> inhibits C. albicans -induced stimulation of the danger response in vaginal epithelium. A431 vaginal epithelial cells were infected with wild-type C. albicans (SC5314) for 3 h (A) or 24 h (B to D) in the absence or presence of 1 or 10 μM
    Clotrimazole, supplied by Bayer AG, used in various techniques. Bioz Stars score: 92/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Valiant clotrimazole
    Effect of pharmacological inhibitors on the basal jejunum I sc . ( A ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 100 μM <t>clotrimazole</t> (post), in lean (open bars) and ob/ob (solid bars) mice. ( B ) Percent inhibition of basal I sc by clotrimazole (100 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( C ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 200 μM DIDS (post), in lean (open bars) and ob/ob (solid bars) mice. ( D ) Percent inhibition of basal I sc by DIDS (200 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( E ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after basolateral application of 100 μM ouabain (post), in lean (open bars) and ob/ob (solid bars) mice. ( F ) Percent inhibition of basal I sc by ouabain (100 μM, basolateral), on lean (open bars) and ob/ob mice (solid black bar). Notes: Values are expressed as mean ± SEM (n=13–18). *Denotes significant difference from lean ( P
    Clotrimazole, supplied by Valiant, used in various techniques. Bioz Stars score: 92/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Schering-Plough clotrimazole
    Effect of pharmacological inhibitors on the basal jejunum I sc . ( A ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 100 μM <t>clotrimazole</t> (post), in lean (open bars) and ob/ob (solid bars) mice. ( B ) Percent inhibition of basal I sc by clotrimazole (100 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( C ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 200 μM DIDS (post), in lean (open bars) and ob/ob (solid bars) mice. ( D ) Percent inhibition of basal I sc by DIDS (200 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( E ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after basolateral application of 100 μM ouabain (post), in lean (open bars) and ob/ob (solid bars) mice. ( F ) Percent inhibition of basal I sc by ouabain (100 μM, basolateral), on lean (open bars) and ob/ob mice (solid black bar). Notes: Values are expressed as mean ± SEM (n=13–18). *Denotes significant difference from lean ( P
    Clotrimazole, supplied by Schering-Plough, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Activation of NF-κB antagonizes SXR signaling and inhibits expression of the SXR target gene CYP3A4. ( A ) HepG2 cells were transfected with SXR-dependent reporter (XREM-LUC) with control or SXR expression vectors. Cells were treated with 10 μM RIF in the presence or absence of TPA (0.1 μM). ( B ) p65 inhibits SXR transactivation and IκBαM rescues p65-mediated inhibition of SXR-dependent reporter gene activation. p65 or IκBαM was used at a 1:1 ratio with SXR expression vector. After transfection, cells were treated with 10 μM RIF, clotrimazole, or RU486 for 24 hours before the assay. ( C ) Human primary hepatocytes and ( D and E ) LS180 cells were treated for 24 hours with 10 μM RIF, clotrimazole, or RU486 in the presence or absence of 0.1 μM TPA or 10 ng/ml TNF-α, as indicated. ( F ) Mouse primary hepatocytes were treated for 24 hours with 10 μM PCN in the presence or absence of 10 ng/ml mouse TNF-α. Total RNAs were isolated, and expression of human CYP3A4 and SXR genes as well as mouse CYP3A11 gene was determined by QRT-PCR assays.

    Journal: The Journal of Clinical Investigation

    Article Title: Mutual repression between steroid and xenobiotic receptor and NF-?B signaling pathways links xenobiotic metabolism and inflammation

    doi: 10.1172/JCI26283

    Figure Lengend Snippet: Activation of NF-κB antagonizes SXR signaling and inhibits expression of the SXR target gene CYP3A4. ( A ) HepG2 cells were transfected with SXR-dependent reporter (XREM-LUC) with control or SXR expression vectors. Cells were treated with 10 μM RIF in the presence or absence of TPA (0.1 μM). ( B ) p65 inhibits SXR transactivation and IκBαM rescues p65-mediated inhibition of SXR-dependent reporter gene activation. p65 or IκBαM was used at a 1:1 ratio with SXR expression vector. After transfection, cells were treated with 10 μM RIF, clotrimazole, or RU486 for 24 hours before the assay. ( C ) Human primary hepatocytes and ( D and E ) LS180 cells were treated for 24 hours with 10 μM RIF, clotrimazole, or RU486 in the presence or absence of 0.1 μM TPA or 10 ng/ml TNF-α, as indicated. ( F ) Mouse primary hepatocytes were treated for 24 hours with 10 μM PCN in the presence or absence of 10 ng/ml mouse TNF-α. Total RNAs were isolated, and expression of human CYP3A4 and SXR genes as well as mouse CYP3A11 gene was determined by QRT-PCR assays.

    Article Snippet: RIF, DEX, RU486, clotrimazole, recombinant human TNF-α, and TPA were purchased from Sigma-Aldrich.

    Techniques: Activation Assay, Expressing, Transfection, Inhibition, Plasmid Preparation, Isolation, Quantitative RT-PCR

    Schematic representation of the proposed signaling mechanism underlying cell death regulated by Ca 2+ entry via redox-sensitive TRPV1, TRPC1, TRPM2, and TRPM7 channels activated by APAP overdose in HepG2 . TRPV1 and TRPC1 channels are activated by oxidative modification of free sulfhydryl groups of cysteine residues, which APAP is able to reach to enhance activation. Initial Ca 2+ influx by APAP-induced ROS induces the mitochondrial and nuclear damages mediating the release of ADPR, which is released into the cytosol to activate TRPM2. ROS activates TRPM7. Suppression of TRPV1, TRPC1, TRPM2, and TRPM7 using blockers, siRNAs and ROS scavengers (NAC or tiron) alleviates APAP-induced Ca 2+ entry and HepG2 death. APAP, N-acetyl-para-aminophenol; [Ca 2+ ] i , calcium ions; HepG2, human hepatoma cell line; TRP, transient receptor potential channels; TRPV1, type 1 vanilloid receptor; TRPC1, type 1 canonical receptor; TRPM2, type 2 melastatin receptor; TRPM7, type 7 melastatin receptor; CaMs, calmodulins; CPZ, capsazepine (TRPV1 antagonist); 2-APB, 2-aminoethyl diphenylborinate (TRPC1 antagonist); CTZ, clotrimazole (TRPM2 antagonist); AA861, 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (TRPM7 antagonist); CsA, cyclosporine A (inhibitor of mitochondrial permeability transition, MPT); H 2 O 2 , hydrogen peroxide; O 2 − , superoxide anion; ROS, reactive oxygen species; GSH, glutathione; ADPR, adenosine diphosphate ribose; JNK, c-jun NH2-terminal kinase; NAC, N-acetyl-L-cysteine.

    Journal: Frontiers in Pharmacology

    Article Title: Different Contribution of Redox-Sensitive Transient Receptor Potential Channels to Acetaminophen-Induced Death of Human Hepatoma Cell Line

    doi: 10.3389/fphar.2016.00019

    Figure Lengend Snippet: Schematic representation of the proposed signaling mechanism underlying cell death regulated by Ca 2+ entry via redox-sensitive TRPV1, TRPC1, TRPM2, and TRPM7 channels activated by APAP overdose in HepG2 . TRPV1 and TRPC1 channels are activated by oxidative modification of free sulfhydryl groups of cysteine residues, which APAP is able to reach to enhance activation. Initial Ca 2+ influx by APAP-induced ROS induces the mitochondrial and nuclear damages mediating the release of ADPR, which is released into the cytosol to activate TRPM2. ROS activates TRPM7. Suppression of TRPV1, TRPC1, TRPM2, and TRPM7 using blockers, siRNAs and ROS scavengers (NAC or tiron) alleviates APAP-induced Ca 2+ entry and HepG2 death. APAP, N-acetyl-para-aminophenol; [Ca 2+ ] i , calcium ions; HepG2, human hepatoma cell line; TRP, transient receptor potential channels; TRPV1, type 1 vanilloid receptor; TRPC1, type 1 canonical receptor; TRPM2, type 2 melastatin receptor; TRPM7, type 7 melastatin receptor; CaMs, calmodulins; CPZ, capsazepine (TRPV1 antagonist); 2-APB, 2-aminoethyl diphenylborinate (TRPC1 antagonist); CTZ, clotrimazole (TRPM2 antagonist); AA861, 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (TRPM7 antagonist); CsA, cyclosporine A (inhibitor of mitochondrial permeability transition, MPT); H 2 O 2 , hydrogen peroxide; O 2 − , superoxide anion; ROS, reactive oxygen species; GSH, glutathione; ADPR, adenosine diphosphate ribose; JNK, c-jun NH2-terminal kinase; NAC, N-acetyl-L-cysteine.

    Article Snippet: Reagents N-acetyl-para-aminophenol (APAP), capsazepine (CPZ), 2-aminoethyl diphenylborinate (2-APB), clotrimazole (CTZ), 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (AA861), N-acetyl-L-cysteine (NAC), dimethylfumarate (DMF), metaphosphoric acid, triethanolamine, and cyclosporine A (CsA) were from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Modification, Activation Assay, Permeability

    Inhibition of APAP- or H 2 O 2 -induced Ca 2+ entry and ROS production by selective TRP channel blockers in HepG2 cells . (A) Effects of selective blockers capsazepine (CPZ; 10 μM) for TRPV1, 2-APB (100 μM) for TRPC1, clotrimazole (CTZ; 50 μM) for TRPM2, or AA861 (10 μM) for TRPM7 on [Ca 2+ ] i rises evoked by APAP (20 mM). Average time courses (left) and Δ[Ca 2+ ] i (right) ( n = 18–57). (B) Effects of 10 μM CPZ, 100 μM 2-APB, 50 μM CTZ, and 10 μM AA861 on [Ca 2+ ] i rises evoked by H 2 O 2 (1 mM). Average time courses (left) and Δ[Ca 2+ ] i (right) ( n = 19–43). (C,D) Effects of selective blockers of TRP channels on ROS production evoked by APAP (20 mM) (C) or H 2 O 2 (1 mM) (D) . Blockers are applied for 3 h before and during APAP or H 2 O 2 stimulation. Data points are mean ± SEM. *** P

    Journal: Frontiers in Pharmacology

    Article Title: Different Contribution of Redox-Sensitive Transient Receptor Potential Channels to Acetaminophen-Induced Death of Human Hepatoma Cell Line

    doi: 10.3389/fphar.2016.00019

    Figure Lengend Snippet: Inhibition of APAP- or H 2 O 2 -induced Ca 2+ entry and ROS production by selective TRP channel blockers in HepG2 cells . (A) Effects of selective blockers capsazepine (CPZ; 10 μM) for TRPV1, 2-APB (100 μM) for TRPC1, clotrimazole (CTZ; 50 μM) for TRPM2, or AA861 (10 μM) for TRPM7 on [Ca 2+ ] i rises evoked by APAP (20 mM). Average time courses (left) and Δ[Ca 2+ ] i (right) ( n = 18–57). (B) Effects of 10 μM CPZ, 100 μM 2-APB, 50 μM CTZ, and 10 μM AA861 on [Ca 2+ ] i rises evoked by H 2 O 2 (1 mM). Average time courses (left) and Δ[Ca 2+ ] i (right) ( n = 19–43). (C,D) Effects of selective blockers of TRP channels on ROS production evoked by APAP (20 mM) (C) or H 2 O 2 (1 mM) (D) . Blockers are applied for 3 h before and during APAP or H 2 O 2 stimulation. Data points are mean ± SEM. *** P

    Article Snippet: Reagents N-acetyl-para-aminophenol (APAP), capsazepine (CPZ), 2-aminoethyl diphenylborinate (2-APB), clotrimazole (CTZ), 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (AA861), N-acetyl-L-cysteine (NAC), dimethylfumarate (DMF), metaphosphoric acid, triethanolamine, and cyclosporine A (CsA) were from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Inhibition

    Curves relating the fluorescence-based fungal growth quotient of an isolate of T. mentagrophytes (IFM 45828) to the concentrations of amorolfine (■) and clotrimazole (●) in the keratin-impregnation antifungal susceptibility test. The dotted line indicates the 0.05 fungal growth quotient inhibition threshold.

    Journal: Journal of Clinical Microbiology

    Article Title: Fluorometric Assessment of In Vitro Antidermatophytic Activities of Antimycotics Based on Their Keratin-Penetrating Power

    doi:

    Figure Lengend Snippet: Curves relating the fluorescence-based fungal growth quotient of an isolate of T. mentagrophytes (IFM 45828) to the concentrations of amorolfine (■) and clotrimazole (●) in the keratin-impregnation antifungal susceptibility test. The dotted line indicates the 0.05 fungal growth quotient inhibition threshold.

    Article Snippet: Amorolfine powder was a gift from Kyorin Pharmaceutical Co. Ltd. (Tokyo, Japan), and clotrimazole powder was purchased from Sigma Chemical Co. (St. Louis, Mo.).

    Techniques: Fluorescence, Inhibition

    Curves relating the fluorescence-based fungal growth quotient for an isolate of T. mentagrophytes (IFM 45828) to concentrations of amorolfine (■) and clotrimazole (▴) in the conventional broth microdilution antifungal susceptibility test. The dotted line indicates the 0.05 fungal growth quotient inhibition threshold.

    Journal: Journal of Clinical Microbiology

    Article Title: Fluorometric Assessment of In Vitro Antidermatophytic Activities of Antimycotics Based on Their Keratin-Penetrating Power

    doi:

    Figure Lengend Snippet: Curves relating the fluorescence-based fungal growth quotient for an isolate of T. mentagrophytes (IFM 45828) to concentrations of amorolfine (■) and clotrimazole (▴) in the conventional broth microdilution antifungal susceptibility test. The dotted line indicates the 0.05 fungal growth quotient inhibition threshold.

    Article Snippet: Amorolfine powder was a gift from Kyorin Pharmaceutical Co. Ltd. (Tokyo, Japan), and clotrimazole powder was purchased from Sigma Chemical Co. (St. Louis, Mo.).

    Techniques: Fluorescence, Inhibition

    Representative micrographs of U251 (A-D) and U87 (E-H) cells grown in the presence of BK and IK1 blockers. Cells were grown in the serum-free OptiMEM media supplemented with serum substitute B27. The BK blocker paxilline (10 µM) and the IK1 inhibitor clotrimazole (10 µM) were added as indicated. Images of the cells were captured ∼48 hrs after addition of channel blockers using Hoffman modulation contrast optics in Olympus IX71 microscope at 10×10 magnification.

    Journal: PLoS ONE

    Article Title: Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

    doi: 10.1371/journal.pone.0012304

    Figure Lengend Snippet: Representative micrographs of U251 (A-D) and U87 (E-H) cells grown in the presence of BK and IK1 blockers. Cells were grown in the serum-free OptiMEM media supplemented with serum substitute B27. The BK blocker paxilline (10 µM) and the IK1 inhibitor clotrimazole (10 µM) were added as indicated. Images of the cells were captured ∼48 hrs after addition of channel blockers using Hoffman modulation contrast optics in Olympus IX71 microscope at 10×10 magnification.

    Article Snippet: Materials Clotrimazole, paxilline, penitrem A, 8,14-Diaza-1,7(1,4)-diquinolinacyclotetradecaphane trifluoroacetate salt (UCL1848), and all other salts and chemicals were from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted.

    Techniques: Microscopy

    Blockers of the Ca 2+ -activated potassium channels BK and IK1 suppress proliferation of U251 cells in a dose dependent fashion. ( A ) Dose response curves for the effects of the BK channel inhibitors, paxilline and penitrem A, on proliferation of U251 cells. Arrow indicates concentration of paxilline that was used to block K + currents in the electrophysiology experiments presented in ( D ). ( B ) Dose response curves for the effects of the IK1 channel inhibitors, clotrimazole and TRAM-34, on proliferation of U251 cells. Arrow indicates concentration of clotrimazole that was used to block K + currents in the electrophysiological experiments presented in ( E ). ( C ) Dose response curves for the effects of the selective SK1-3 channel blocker UCL1848 on proliferation of U251 cells. ( D ) Effect of the “aged” paxilline on the whole-cell BK currents. Cell proliferation medium containing 10 µM paxilline was collected after 24-hr incubation in cell proliferation assays, diluted 10-fold with electrophysiological bath solution, and used for inhibiting BK currents. Nominal concentration of paxilline was 1 µM (indicated by arrow in ( A ), to compare proliferation and electrophysiology data). Representative of three experiments. ( E ) Effect of the “aged” clotrimazole on the whole-cell IK1 currents. Cell proliferation medium containing 10 µM clotrimazole was collected after 24-hr incubation in cell proliferation assays, diluted 10-fold, and used for inhibiting IK1 currents. Nominal concentration of clotrimazole was 1 µM (indicated by arrow in ( B )). Representative of three experiments. ( F ) Comparison of normalized effects of the “aged” paxilline and clotrimazole on the whole cell K + currents to their effects on cell proliferation. Inhibition of BK and IK1 currents was calculated as average inhibition of the whole K + cell currents at +140 and 0 mV for BK and IK1, respectively.

    Journal: PLoS ONE

    Article Title: Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

    doi: 10.1371/journal.pone.0012304

    Figure Lengend Snippet: Blockers of the Ca 2+ -activated potassium channels BK and IK1 suppress proliferation of U251 cells in a dose dependent fashion. ( A ) Dose response curves for the effects of the BK channel inhibitors, paxilline and penitrem A, on proliferation of U251 cells. Arrow indicates concentration of paxilline that was used to block K + currents in the electrophysiology experiments presented in ( D ). ( B ) Dose response curves for the effects of the IK1 channel inhibitors, clotrimazole and TRAM-34, on proliferation of U251 cells. Arrow indicates concentration of clotrimazole that was used to block K + currents in the electrophysiological experiments presented in ( E ). ( C ) Dose response curves for the effects of the selective SK1-3 channel blocker UCL1848 on proliferation of U251 cells. ( D ) Effect of the “aged” paxilline on the whole-cell BK currents. Cell proliferation medium containing 10 µM paxilline was collected after 24-hr incubation in cell proliferation assays, diluted 10-fold with electrophysiological bath solution, and used for inhibiting BK currents. Nominal concentration of paxilline was 1 µM (indicated by arrow in ( A ), to compare proliferation and electrophysiology data). Representative of three experiments. ( E ) Effect of the “aged” clotrimazole on the whole-cell IK1 currents. Cell proliferation medium containing 10 µM clotrimazole was collected after 24-hr incubation in cell proliferation assays, diluted 10-fold, and used for inhibiting IK1 currents. Nominal concentration of clotrimazole was 1 µM (indicated by arrow in ( B )). Representative of three experiments. ( F ) Comparison of normalized effects of the “aged” paxilline and clotrimazole on the whole cell K + currents to their effects on cell proliferation. Inhibition of BK and IK1 currents was calculated as average inhibition of the whole K + cell currents at +140 and 0 mV for BK and IK1, respectively.

    Article Snippet: Materials Clotrimazole, paxilline, penitrem A, 8,14-Diaza-1,7(1,4)-diquinolinacyclotetradecaphane trifluoroacetate salt (UCL1848), and all other salts and chemicals were from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted.

    Techniques: Concentration Assay, Blocking Assay, Incubation, Inhibition

    IK1 channels are functionally expressed in U251 glioma cells. ( A ) Representative recordings of the whole-cell IK1 currents elicited by depolarization step pulses from −120 mV to +80 mV in 20 mV intervals. Whole cell IK1 currents were activated by clamping pipette [Ca 2+ ] at 750 nM. To prevent concomitant activation of BK currents, 2 µM paxilline was added into bath solution. ( B ) In the same cell shown in ( A ), the whole cell IK1 currents were inhibited by the potent IK1 blocker clotrimazole (2 µM). ( C ) Whole cell currents in response to depolarization ramps from −120 mV to +80 mV in the absence or presence of clotrimazole. ( D–F ) Results of similar experiments employing the selective IK1 blocker TRAM-34 (1 µM).

    Journal: PLoS ONE

    Article Title: Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

    doi: 10.1371/journal.pone.0012304

    Figure Lengend Snippet: IK1 channels are functionally expressed in U251 glioma cells. ( A ) Representative recordings of the whole-cell IK1 currents elicited by depolarization step pulses from −120 mV to +80 mV in 20 mV intervals. Whole cell IK1 currents were activated by clamping pipette [Ca 2+ ] at 750 nM. To prevent concomitant activation of BK currents, 2 µM paxilline was added into bath solution. ( B ) In the same cell shown in ( A ), the whole cell IK1 currents were inhibited by the potent IK1 blocker clotrimazole (2 µM). ( C ) Whole cell currents in response to depolarization ramps from −120 mV to +80 mV in the absence or presence of clotrimazole. ( D–F ) Results of similar experiments employing the selective IK1 blocker TRAM-34 (1 µM).

    Article Snippet: Materials Clotrimazole, paxilline, penitrem A, 8,14-Diaza-1,7(1,4)-diquinolinacyclotetradecaphane trifluoroacetate salt (UCL1848), and all other salts and chemicals were from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted.

    Techniques: Transferring, Activation Assay

    Effects of the BK blocker paxilline and the IK blocker clotrimazole on U251 cell proliferation in serum-containing and serum-free media. Paxilline (10 µM) and clotrimazole (10 µM) were added to culture media alone or in combination, and rates of cell proliferation were determined 48 hrs later using an MTT proliferation assay. Proliferation assays were performed in standard cell culture medium (DMEM +10% FBS), serum-free OptiMEM medium supplemented with serum substitute B27, or in OptiMEM+B27 additionally containing bovine serum albumin (2 mg/ml). Quantitatively similar data were obtained using Coulter counter assay (see Fig. S2 ). *, p

    Journal: PLoS ONE

    Article Title: Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

    doi: 10.1371/journal.pone.0012304

    Figure Lengend Snippet: Effects of the BK blocker paxilline and the IK blocker clotrimazole on U251 cell proliferation in serum-containing and serum-free media. Paxilline (10 µM) and clotrimazole (10 µM) were added to culture media alone or in combination, and rates of cell proliferation were determined 48 hrs later using an MTT proliferation assay. Proliferation assays were performed in standard cell culture medium (DMEM +10% FBS), serum-free OptiMEM medium supplemented with serum substitute B27, or in OptiMEM+B27 additionally containing bovine serum albumin (2 mg/ml). Quantitatively similar data were obtained using Coulter counter assay (see Fig. S2 ). *, p

    Article Snippet: Materials Clotrimazole, paxilline, penitrem A, 8,14-Diaza-1,7(1,4)-diquinolinacyclotetradecaphane trifluoroacetate salt (UCL1848), and all other salts and chemicals were from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted.

    Techniques: MTT Assay, Proliferation Assay, Cell Culture

    Functional expression of BK and IK1 channels in primary cells derived from glioblastoma multiforme (GBM). ( A ) Representative recordings of macroscopic BK currents in primary cells cultured from surgical sample of glioblastoma multiforme. Currents were elicited by step pulses from −80 mV to +140 mV. ( B ) In the same cell shown in ( A ), the BK blocker paxilline (2 µM) potently inhibited macroscopic K + currents. ( C ) Representative traces of K + currents elicited in response to depolarization ramps from −80 mV to +140 mV in the absence and presence of paxilline. ( D ) Representative recordings of the whole-cell IK1 currents activated by step pulses from −120 to +60 mV. To isolate IK1 currents, [Ca 2+ ] pipette was clamped at 750 nM and 2 µM paxilline was added into bath solution. ( E ) The specific IK1 inhibitor clotrimazole (2 µM) potently suppressed macroscopic K + currents. ( F ) Representative traces of K + currents elicited in response to depolarization ramps −120 mV to +60 mV in the absence and presence of clotrimazole. For additional experimental details, see legend to Fig. 2 and Results section.

    Journal: PLoS ONE

    Article Title: Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

    doi: 10.1371/journal.pone.0012304

    Figure Lengend Snippet: Functional expression of BK and IK1 channels in primary cells derived from glioblastoma multiforme (GBM). ( A ) Representative recordings of macroscopic BK currents in primary cells cultured from surgical sample of glioblastoma multiforme. Currents were elicited by step pulses from −80 mV to +140 mV. ( B ) In the same cell shown in ( A ), the BK blocker paxilline (2 µM) potently inhibited macroscopic K + currents. ( C ) Representative traces of K + currents elicited in response to depolarization ramps from −80 mV to +140 mV in the absence and presence of paxilline. ( D ) Representative recordings of the whole-cell IK1 currents activated by step pulses from −120 to +60 mV. To isolate IK1 currents, [Ca 2+ ] pipette was clamped at 750 nM and 2 µM paxilline was added into bath solution. ( E ) The specific IK1 inhibitor clotrimazole (2 µM) potently suppressed macroscopic K + currents. ( F ) Representative traces of K + currents elicited in response to depolarization ramps −120 mV to +60 mV in the absence and presence of clotrimazole. For additional experimental details, see legend to Fig. 2 and Results section.

    Article Snippet: Materials Clotrimazole, paxilline, penitrem A, 8,14-Diaza-1,7(1,4)-diquinolinacyclotetradecaphane trifluoroacetate salt (UCL1848), and all other salts and chemicals were from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted.

    Techniques: Functional Assay, Expressing, Derivative Assay, Cell Culture, Transferring

    (A) Dose-concentration curve for Cx50 inhibition by clotrimazole. (B) Connexin-selectivity profile of clotrimazole (10 μM). Shown is percentage of current inhibition (mean ± SEM).

    Journal: Frontiers in Pharmacology

    Article Title: Triarylmethanes, a New Class of Cx50 Inhibitors

    doi: 10.3389/fphar.2012.00106

    Figure Lengend Snippet: (A) Dose-concentration curve for Cx50 inhibition by clotrimazole. (B) Connexin-selectivity profile of clotrimazole (10 μM). Shown is percentage of current inhibition (mean ± SEM).

    Article Snippet: Chemicals and reagents Clotrimazole (CAS No. 23593-75-1), triphenylmethane (CAS No. 519-73-3), triphenylmethyl chloride (CAS No. 76-83-5), triphenylmethanol (CAS No. 76-84-6), 3,3,3-triphenylpropionic acid (T51, CAS No. 900-91-4), (R )-(+)-α,α-diphenyl-2-pyrrolidinemethanol (T52, CAS No. 22348-32-9), (S )-(−)-α,α-diphenyl-2-pyrrolidinemethanol (T53, CAS No. 112068-01-6), diphenyl-4-pyridylmethane (T160, CAS No. 3678-72-6), and triphenylmethylamine (T162, CAS No. 5824-40-8) were purchased from Sigma-Aldrich (St. Louis, MO).

    Techniques: Concentration Assay, Inhibition

    Time course of the effect of PAA-10, astemizole, clotrimazole, and rutin on the junctional currents of Cx50 channels expressed in N2A cell pairs measured by dual whole-cell patch-clamp .

    Journal: Frontiers in Pharmacology

    Article Title: Triarylmethanes, a New Class of Cx50 Inhibitors

    doi: 10.3389/fphar.2012.00106

    Figure Lengend Snippet: Time course of the effect of PAA-10, astemizole, clotrimazole, and rutin on the junctional currents of Cx50 channels expressed in N2A cell pairs measured by dual whole-cell patch-clamp .

    Article Snippet: Chemicals and reagents Clotrimazole (CAS No. 23593-75-1), triphenylmethane (CAS No. 519-73-3), triphenylmethyl chloride (CAS No. 76-83-5), triphenylmethanol (CAS No. 76-84-6), 3,3,3-triphenylpropionic acid (T51, CAS No. 900-91-4), (R )-(+)-α,α-diphenyl-2-pyrrolidinemethanol (T52, CAS No. 22348-32-9), (S )-(−)-α,α-diphenyl-2-pyrrolidinemethanol (T53, CAS No. 112068-01-6), diphenyl-4-pyridylmethane (T160, CAS No. 3678-72-6), and triphenylmethylamine (T162, CAS No. 5824-40-8) were purchased from Sigma-Aldrich (St. Louis, MO).

    Techniques: Patch Clamp

    Effects of K Ca channel blockers on Gly‐Sar‐stimulated jejunal Isc response in mice. Inhibitory effect of TRAM‐34, Clotrimazole, lberiotoxin and Apamin on the time course of Gly‐Sar stimulated jejunal mucosal I sc (a–d). Gly‐Sar was added to mucosal side after TRAM‐34 (10 μM) Clotrimazole (30 μM), lberiotoxin (100 nM) or Apamin (100 nM) were added to different sides of the tissues for 20 min (e–h). (d, f and h) Summarize the data comparing the effects of Ca 2+ omission plus TRAM‐34, Clotrimazole, lberiotoxin and Apamin on Gly‐Sar‐induced ∆ I sc. Data are given as mean ± SEM ( n = 5 in each series), * p

    Journal: Physiological Reports

    Article Title: Calcium‐sensing receptor regulates intestinal dipeptide absorption via Ca2+ signaling and IKCa activation, et al. Calcium‐sensing receptor regulates intestinal dipeptide absorption via Ca2+ signaling and IKCa activation

    doi: 10.14814/phy2.14337

    Figure Lengend Snippet: Effects of K Ca channel blockers on Gly‐Sar‐stimulated jejunal Isc response in mice. Inhibitory effect of TRAM‐34, Clotrimazole, lberiotoxin and Apamin on the time course of Gly‐Sar stimulated jejunal mucosal I sc (a–d). Gly‐Sar was added to mucosal side after TRAM‐34 (10 μM) Clotrimazole (30 μM), lberiotoxin (100 nM) or Apamin (100 nM) were added to different sides of the tissues for 20 min (e–h). (d, f and h) Summarize the data comparing the effects of Ca 2+ omission plus TRAM‐34, Clotrimazole, lberiotoxin and Apamin on Gly‐Sar‐induced ∆ I sc. Data are given as mean ± SEM ( n = 5 in each series), * p

    Article Snippet: Iberiotoxin and Clotrimazole were purchased from Tocris (Shanghai, China).

    Techniques: Mouse Assay

    NDSB cosolubilization relieves the artificial inhibition of enzymatic activity. The aggregation-prone compounds, I4PTH (0.2 m m ; ▪), clotrimazole (0.4 m m ; ▪), and benzyl benzoate (1.0 m m ; ▪), were added to the reaction solutions of the chymotrypsin assays with the indicated concentrations of NDSB256. The bars indicate the amount of product in the presence of the aggregation-prone compounds relative to that in the absence of the aggregation-prone compounds.

    Journal: Chemmedchem

    Article Title: Suppression of Problematic Compound Oligomerization by Cosolubilization of Nondetergent Sulfobetaines

    doi: 10.1002/cmdc.201500057

    Figure Lengend Snippet: NDSB cosolubilization relieves the artificial inhibition of enzymatic activity. The aggregation-prone compounds, I4PTH (0.2 m m ; ▪), clotrimazole (0.4 m m ; ▪), and benzyl benzoate (1.0 m m ; ▪), were added to the reaction solutions of the chymotrypsin assays with the indicated concentrations of NDSB256. The bars indicate the amount of product in the presence of the aggregation-prone compounds relative to that in the absence of the aggregation-prone compounds.

    Article Snippet: Clotrimazole was purchased from Wako (Tokyo, Japan).

    Techniques: Inhibition, Activity Assay

    Clotrimazole inhibits C. albicans -induced stimulation of the danger response in vaginal epithelium. A431 vaginal epithelial cells were infected with wild-type C. albicans (SC5314) for 3 h (A) or 24 h (B to D) in the absence or presence of 1 or 10 μM

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Clotrimazole Dampens Vaginal Inflammation and Neutrophil Infiltration in Response to Candida albicans Infection

    doi: 10.1128/AAC.01244-13

    Figure Lengend Snippet: Clotrimazole inhibits C. albicans -induced stimulation of the danger response in vaginal epithelium. A431 vaginal epithelial cells were infected with wild-type C. albicans (SC5314) for 3 h (A) or 24 h (B to D) in the absence or presence of 1 or 10 μM

    Article Snippet: Infections of vaginal epithelial cell line A431 with C. albicans strain SC5314 in the absence or presence of 1 μM or 10 μM clotrimazole (Bayer AG) were performed as previously described ( ).

    Techniques: Infection

    Clotrimazole blocks neutrophil infiltration to C. albicans -infected vaginal epithelium. A431 vaginal epithelial cells were infected with wild-type C. albicans (SC5314) for 24 h in the absence or presence of 10 μM clotrimazole. The supernatants

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Clotrimazole Dampens Vaginal Inflammation and Neutrophil Infiltration in Response to Candida albicans Infection

    doi: 10.1128/AAC.01244-13

    Figure Lengend Snippet: Clotrimazole blocks neutrophil infiltration to C. albicans -infected vaginal epithelium. A431 vaginal epithelial cells were infected with wild-type C. albicans (SC5314) for 24 h in the absence or presence of 10 μM clotrimazole. The supernatants

    Article Snippet: Infections of vaginal epithelial cell line A431 with C. albicans strain SC5314 in the absence or presence of 1 μM or 10 μM clotrimazole (Bayer AG) were performed as previously described ( ).

    Techniques: Infection

    Effect of pharmacological inhibitors on the basal jejunum I sc . ( A ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 100 μM clotrimazole (post), in lean (open bars) and ob/ob (solid bars) mice. ( B ) Percent inhibition of basal I sc by clotrimazole (100 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( C ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 200 μM DIDS (post), in lean (open bars) and ob/ob (solid bars) mice. ( D ) Percent inhibition of basal I sc by DIDS (200 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( E ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after basolateral application of 100 μM ouabain (post), in lean (open bars) and ob/ob (solid bars) mice. ( F ) Percent inhibition of basal I sc by ouabain (100 μM, basolateral), on lean (open bars) and ob/ob mice (solid black bar). Notes: Values are expressed as mean ± SEM (n=13–18). *Denotes significant difference from lean ( P

    Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

    Article Title: Decreased basal chloride secretion and altered cystic fibrosis transmembrane conductance regulatory protein, Villin, GLUT5 protein expression in jejunum from leptin-deficient mice

    doi: 10.2147/DMSO.S63714

    Figure Lengend Snippet: Effect of pharmacological inhibitors on the basal jejunum I sc . ( A ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 100 μM clotrimazole (post), in lean (open bars) and ob/ob (solid bars) mice. ( B ) Percent inhibition of basal I sc by clotrimazole (100 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( C ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after bilateral application of 200 μM DIDS (post), in lean (open bars) and ob/ob (solid bars) mice. ( D ) Percent inhibition of basal I sc by DIDS (200 μM, bilateral), on lean (open bars) and ob/ob mice (solid black bar). ( E ) Average initial steady state basal I sc (pre) and resulting basal I sc 15 minutes after basolateral application of 100 μM ouabain (post), in lean (open bars) and ob/ob (solid bars) mice. ( F ) Percent inhibition of basal I sc by ouabain (100 μM, basolateral), on lean (open bars) and ob/ob mice (solid black bar). Notes: Values are expressed as mean ± SEM (n=13–18). *Denotes significant difference from lean ( P

    Article Snippet: Clotrimazole was purchased from MP Biomedicals (Santa Ana, CA, USA).

    Techniques: Mouse Assay, Inhibition