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  • dmso  (ATCC)
    99
    ATCC dmso
    Dmso, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 619 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher pluronic f 127
    Pluronic F 127, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 5795 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore dimethyl sulfoxide dmso
    Dimethyl Sulfoxide Dmso, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 20263 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore dmso
    Dmso, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 55308 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher to pro 3 iodide 642 661 1 mm solution in dmso
    To Pro 3 Iodide 642 661 1 Mm Solution In Dmso, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 2169 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher sybr gold nucleic acid gel stain
    Sybr Gold Nucleic Acid Gel Stain, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 3657 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher dimethyl sulfoxide dmso
    Heat map of <t>panobinostat</t> -induced gene expression changes in MDA-MB-231, MDA-MB-468, and MCF-7 cells . MDA-MB-231, MDA-MB-468, or MCF-7 cells were treated for 24 hours with panobinostat (100 nM) or vehicle <t>(DMSO)</t> and then assayed via the Human Breast Cancer and Estrogen Receptor Signaling RT 2 Profiler™ PCR Array. Red signifies up-regulation and green signifies down-regulation by panobinostat compared to MDA-MB-231 vehicle treated controls. Data are representative of three independent experiments. Genes regulated at least 2-fold are also summarized in Additional file 1 (MDA-MB-231), 2 (MDA-MB-468) and 3 (MCF-7). DMSO, dimethyl sulfoxide.
    Dimethyl Sulfoxide Dmso, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 2578 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Fisher Scientific dmso
    Survivin antagonists cooperate with radiation and LDE225 SHH antagonists A) Tumor cells were treated with either 0.1% <t>DMSO,</t> 50 nM <t>YM155,</t> or 10 μg/ml S12 for 24 hr, and then irradiated with 0, 0.25, or 0.5 gray (Gy). After 24 hr, cells were pulsed with 3 H-thymidine and assayed for incorporation. Treatment with antagonists enhanced sensitivity of tumor cells to radiation (p
    Dmso, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 93/100, based on 1380 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Merck KGaA dmso
    HSulf-1 in combination with <t>palbociclib</t> exerts synergistic antitumor effects by inducing G 1 /S stage cell cycle arrest and by inhibiting migration, invasion and epithelial-mesenchymal transition in vitro . (A-E) Hs578T and MDA-MB-231 cells following transient transfection with the control vector or HSulf-1 overexpression plasmids and incubation with 500 nM palbociclib or <t>DMSO</t> for 72 h. (A) Cell cycle analysis. G 1 and S phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-Vector+Palbociclib; G 1 and G 2 phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-HSulf-1+Vehicle; G 1 phase of pcDNA3.0-Vector+Palbociclib vs. pcDNA3.0-HSulf-1+Palbociclib; G 1 phase of pcDNA3.0-HSulf-1+Vehicle vs. pcDNA3.0-HSulf-1+Palbociclib. (B) Apoptosis analysis. (C) Wound healing assays. (D) Transwell assays. Magnification, x100. (E) Western blotting was performed to measure E-cadherin, vimentin and N-cadherin expression, with β-actin used as an internal control. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P
    Dmso, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 94/100, based on 1546 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Merck KGaA dimethyl sulfoxide dmso
    In vivo activity of <t>EN4</t> in a mouse tissue cage model. The numbers of planktonic SA113 (A) and the viability of leukocytes (B) present in tissue cage fluid from cages treated with 100 or 250 μg of EN4 or 30 μg of daptomycin (DAP) and infected with 4 × 10 3 CFU of SA113 were investigated. Open circles indicate control mice injected with 1% <t>DMSO-PBS.</t> The values shown are means ± the SDs.
    Dimethyl Sulfoxide Dmso, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 94/100, based on 813 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Fisher Scientific dimethyl sulfoxide dmso
    Analogs of <t>honokiol</t> do not bind or inhibit FOXM1 a C3-luc cells were induced with doxycycline and treated with the indicated analogs of honokiol at the concentration of 40 µM for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b DU145 prostate cancer cells were treated as indicated. Following treatment cells were collected and immunoblotting was performed for FOXM1, cleaved caspase-3 and β-actin as the loading control. c STD NMR spectra of 2 mM of: (I) 2 mM eugenol, (II) 2 mM O -eugenol, (III) 2 mM 2-allylphenol and (IV) 2 mM 2,2 dihydroxybiphenyl. The chemical structure of each small molecule is illustrated. Signals from vehicle <t>(DMSO)</t> and water are labeled. d STD NMR spectra of 150 ng of recombinant FOXM1 plus: (I) 2 mM eugenol, (II) 2 mM O-eugenol, (III) 2 mM 2,2 dihydroxybiphenyl and (IV) 2 mM 2-allylphenol. The chemical structure of each small molecule is illustrated. STD signals arising from the aryl groups are annotated and signals from vehicle (DMSO) and water are labeled
    Dimethyl Sulfoxide Dmso, supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 93/100, based on 730 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher sytox green nucleic acid stain 5 mm solution in dmso
    Analogs of <t>honokiol</t> do not bind or inhibit FOXM1 a C3-luc cells were induced with doxycycline and treated with the indicated analogs of honokiol at the concentration of 40 µM for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b DU145 prostate cancer cells were treated as indicated. Following treatment cells were collected and immunoblotting was performed for FOXM1, cleaved caspase-3 and β-actin as the loading control. c STD NMR spectra of 2 mM of: (I) 2 mM eugenol, (II) 2 mM O -eugenol, (III) 2 mM 2-allylphenol and (IV) 2 mM 2,2 dihydroxybiphenyl. The chemical structure of each small molecule is illustrated. Signals from vehicle <t>(DMSO)</t> and water are labeled. d STD NMR spectra of 150 ng of recombinant FOXM1 plus: (I) 2 mM eugenol, (II) 2 mM O-eugenol, (III) 2 mM 2,2 dihydroxybiphenyl and (IV) 2 mM 2-allylphenol. The chemical structure of each small molecule is illustrated. STD signals arising from the aryl groups are annotated and signals from vehicle (DMSO) and water are labeled
    Sytox Green Nucleic Acid Stain 5 Mm Solution In Dmso, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1702 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore dimethyl sulfoxide
    Analogs of <t>honokiol</t> do not bind or inhibit FOXM1 a C3-luc cells were induced with doxycycline and treated with the indicated analogs of honokiol at the concentration of 40 µM for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b DU145 prostate cancer cells were treated as indicated. Following treatment cells were collected and immunoblotting was performed for FOXM1, cleaved caspase-3 and β-actin as the loading control. c STD NMR spectra of 2 mM of: (I) 2 mM eugenol, (II) 2 mM O -eugenol, (III) 2 mM 2-allylphenol and (IV) 2 mM 2,2 dihydroxybiphenyl. The chemical structure of each small molecule is illustrated. Signals from vehicle <t>(DMSO)</t> and water are labeled. d STD NMR spectra of 150 ng of recombinant FOXM1 plus: (I) 2 mM eugenol, (II) 2 mM O-eugenol, (III) 2 mM 2,2 dihydroxybiphenyl and (IV) 2 mM 2-allylphenol. The chemical structure of each small molecule is illustrated. STD signals arising from the aryl groups are annotated and signals from vehicle (DMSO) and water are labeled
    Dimethyl Sulfoxide, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 27840 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Merck & Co dmso
    Dose-dependent antifungal effect of <t>L1</t> against Botrytis cinerea B05.10 at 4 °C. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in <t>DMSO</t> (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.
    Dmso, supplied by Merck & Co, used in various techniques. Bioz Stars score: 92/100, based on 970 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore hek293 cells
    DWORF activates SERCA2a in the absence of PLB. (A) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). (B) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF-P15/W22 (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). GFP-SERCA2a was stably expressed in <t>HEK293</t> cells, then 20 μg of DNA per dish (for unlabeled DWORF or unlabeled mutant DWORF) was transiently transfected into the cells. Ca-ATPase assays were performed using cell homogenates as described in Methods. Activity was normalized to the control (SERCA2a only), since DWORF had no significant effect on V max . (n=3)
    Hek293 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 7297 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Carl Roth GmbH dmso
    Treatment with HIT and <t>SAHA</t> results in a reduced proliferation in osteosarcoma xenografts. Histological analysis of proliferation in tumors treated with <t>DMSO</t> (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The proliferation rate was significantly reduced in tumors after treatment with SAHA and HIT at all investigation time points. HIT only treatment led to a significantly lower proliferation rate 8 and 24 days after irradiation compared to the control group. SAHA only treatment had no significant effect on tumor proliferation
    Dmso, supplied by Carl Roth GmbH, used in various techniques. Bioz Stars score: 93/100, based on 622 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Amresco dmso
    <t>Gimatecan</t> Inhibited HCC Cell Growth in Vitro . Different HCC cell lines were cultured and incubated with various concentrations of gimatecan at 37 ºC for 72 hours. The percentages of viable cells were measured at the end the incubation period. 100% refers to the number of cells after 72 hours of incubation in the presence of the vehicle control (0.1% <t>DMSO).</t>
    Dmso, supplied by Amresco, used in various techniques. Bioz Stars score: 93/100, based on 499 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    cayman chemical dmso
    Effects of <t>GYY4137</t> on the rat DLNCs. The DLNCs were isolated from the rats immunized with MOG + CFA. The percentage of CD4+ CD25+ FoxP3+ cells (Treg), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg was determined among the DLNCs ( A ) or among CD4+ T cells purified from the DLNCs ( B ), after 40 min of cultivation in the presence of 200 μM GYY4137 (GYY) or <t>DMSO</t> as the vehicle (DMSO). The percentage of Th17 cells was determined among the DLNCs, treated with GYY4137 (GYY) or DMSO as the vehicle (DMSO) for 40 min and subsequently stimulated for 4 h ( C ). In some experiments, the cultures without DMSO (Ctrl) were also performed ( A , C ). IL-17 and IFN-γ cytokine concentrations in the supernatants of the 24 h cell cultures of MOG re-stimulated DLNCs and treated with GYY4137, were determined by ELISA ( D ). Data are presented as the mean + standard deviation (SD) from three ( C ), four ( B ) or six samples ( A , D ). * p
    Dmso, supplied by cayman chemical, used in various techniques. Bioz Stars score: 93/100, based on 333 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Heat map of panobinostat -induced gene expression changes in MDA-MB-231, MDA-MB-468, and MCF-7 cells . MDA-MB-231, MDA-MB-468, or MCF-7 cells were treated for 24 hours with panobinostat (100 nM) or vehicle (DMSO) and then assayed via the Human Breast Cancer and Estrogen Receptor Signaling RT 2 Profiler™ PCR Array. Red signifies up-regulation and green signifies down-regulation by panobinostat compared to MDA-MB-231 vehicle treated controls. Data are representative of three independent experiments. Genes regulated at least 2-fold are also summarized in Additional file 1 (MDA-MB-231), 2 (MDA-MB-468) and 3 (MCF-7). DMSO, dimethyl sulfoxide.

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Heat map of panobinostat -induced gene expression changes in MDA-MB-231, MDA-MB-468, and MCF-7 cells . MDA-MB-231, MDA-MB-468, or MCF-7 cells were treated for 24 hours with panobinostat (100 nM) or vehicle (DMSO) and then assayed via the Human Breast Cancer and Estrogen Receptor Signaling RT 2 Profiler™ PCR Array. Red signifies up-regulation and green signifies down-regulation by panobinostat compared to MDA-MB-231 vehicle treated controls. Data are representative of three independent experiments. Genes regulated at least 2-fold are also summarized in Additional file 1 (MDA-MB-231), 2 (MDA-MB-468) and 3 (MCF-7). DMSO, dimethyl sulfoxide.

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Expressing, Multiple Displacement Amplification, Polymerase Chain Reaction

    Panobinostat decreases TNBC cell proliferation and viability . Cells from four TNBC cell lines (MDA-MB-157, MDA-MB-231, MDA-MB-468, BT549) and three ER-positive cell lines (MCF-7, MDA-MB-361, ZR-75) were treated with panobinostat (50, 100, 200 nM) or vehicle (DMSO) for 24 hours and assayed by (A) MTT proliferation and (B) trypan blue exclusion assays. Data are represented as percent control (mean ± SEM) of three independent experiments, (**, P

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Panobinostat decreases TNBC cell proliferation and viability . Cells from four TNBC cell lines (MDA-MB-157, MDA-MB-231, MDA-MB-468, BT549) and three ER-positive cell lines (MCF-7, MDA-MB-361, ZR-75) were treated with panobinostat (50, 100, 200 nM) or vehicle (DMSO) for 24 hours and assayed by (A) MTT proliferation and (B) trypan blue exclusion assays. Data are represented as percent control (mean ± SEM) of three independent experiments, (**, P

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Multiple Displacement Amplification, MTT Assay

    Panobinostat induces apoptosis in TNBC cells . (A) TNBC cells treated with panobinostat (100, 200 nM) or vehicle (DMSO) for 24 hours were assayed by DNA fragmentation (Cell Death ELISA) assay to assess changes in apoptosis. Data are presented as enrichment (mean ± SEM) versus control of two independent experiments (***, P

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Panobinostat induces apoptosis in TNBC cells . (A) TNBC cells treated with panobinostat (100, 200 nM) or vehicle (DMSO) for 24 hours were assayed by DNA fragmentation (Cell Death ELISA) assay to assess changes in apoptosis. Data are presented as enrichment (mean ± SEM) versus control of two independent experiments (***, P

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Enzyme-linked Immunosorbent Assay

    Effect of panobinostat on tumor growth in MDA-MB-231 and BT549 xenograft models . Female, CB-17/SCID mice ( n = 5/group) were injected with (A) MDA-MB-231-tRFP or (B) BT-549-tRFP cells (5 × 10 6 cells/injection) bilaterally into the inguinal mammary fat pad. On day 14, mice were treated intraperitoneally (i.p.) with panobinostat (10 mg/kg) or vehicle (1:20 DMSO in normal saline) five days/week for 28 days. Data points represent average tumor volume ± SEM, (***, P

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Effect of panobinostat on tumor growth in MDA-MB-231 and BT549 xenograft models . Female, CB-17/SCID mice ( n = 5/group) were injected with (A) MDA-MB-231-tRFP or (B) BT-549-tRFP cells (5 × 10 6 cells/injection) bilaterally into the inguinal mammary fat pad. On day 14, mice were treated intraperitoneally (i.p.) with panobinostat (10 mg/kg) or vehicle (1:20 DMSO in normal saline) five days/week for 28 days. Data points represent average tumor volume ± SEM, (***, P

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Multiple Displacement Amplification, Mouse Assay, Injection

    Panobinostat up-regulates CDH1 expression and initiates EMT reversal in MDA-MB-231 Cells . MDA-MB-231 cells were plated overnight and treated with panobinostat (100 nM) or vehicle (DMSO) for 24 hours. The expression of CDH1 was examined by (A) flow cytometry and (B) ELISA. Data are represented as mean ± SEM of two independent experiments, (***, P

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Panobinostat up-regulates CDH1 expression and initiates EMT reversal in MDA-MB-231 Cells . MDA-MB-231 cells were plated overnight and treated with panobinostat (100 nM) or vehicle (DMSO) for 24 hours. The expression of CDH1 was examined by (A) flow cytometry and (B) ELISA. Data are represented as mean ± SEM of two independent experiments, (***, P

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Expressing, Multiple Displacement Amplification, Flow Cytometry, Cytometry, Enzyme-linked Immunosorbent Assay

    Panobinostat increases histone H3 (Lys9) and H4 (Lys8) acetylation in TNBC cell lines . Cells were treated with panobinostat (100, 200 nM) or vehicle (DMSO) for 18 hours, fixed, permeabilized and stained for acetyl-histones (A) H3 (Lys9) or (B) H4 (Lys8) and subjected to flow cytometry. Data are presented as mean fluorescence intensity (mean ± SEM) of two independent experiments, (***, P

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

    doi: 10.1186/bcr3192

    Figure Lengend Snippet: Panobinostat increases histone H3 (Lys9) and H4 (Lys8) acetylation in TNBC cell lines . Cells were treated with panobinostat (100, 200 nM) or vehicle (DMSO) for 18 hours, fixed, permeabilized and stained for acetyl-histones (A) H3 (Lys9) or (B) H4 (Lys8) and subjected to flow cytometry. Data are presented as mean fluorescence intensity (mean ± SEM) of two independent experiments, (***, P

    Article Snippet: Panobinostat was dissolved in dimethyl sulfoxide (DMSO) (Invitrogen) as a 1 mM stock solution and kept at -20°C.

    Techniques: Staining, Flow Cytometry, Cytometry, Fluorescence

    Survivin antagonists cooperate with radiation and LDE225 SHH antagonists A) Tumor cells were treated with either 0.1% DMSO, 50 nM YM155, or 10 μg/ml S12 for 24 hr, and then irradiated with 0, 0.25, or 0.5 gray (Gy). After 24 hr, cells were pulsed with 3 H-thymidine and assayed for incorporation. Treatment with antagonists enhanced sensitivity of tumor cells to radiation (p

    Journal: Oncogene

    Article Title: Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma

    doi: 10.1038/onc.2014.304

    Figure Lengend Snippet: Survivin antagonists cooperate with radiation and LDE225 SHH antagonists A) Tumor cells were treated with either 0.1% DMSO, 50 nM YM155, or 10 μg/ml S12 for 24 hr, and then irradiated with 0, 0.25, or 0.5 gray (Gy). After 24 hr, cells were pulsed with 3 H-thymidine and assayed for incorporation. Treatment with antagonists enhanced sensitivity of tumor cells to radiation (p

    Article Snippet: To evaluate Survivin expression after YM155 treatment, tumor cells were plated on 6-well plates (6-8M cells/well) and treated with YM155 or DMSO (Fisher Scientific Inc. San Diego, CA) at 1 μM for 24hrs and processed as described above.

    Techniques: Irradiation

    YM155 inhibits growth of Ptch mutant tumor cells in vivo (A-F) Tumor cells were suspended in GFR matrigel (1:1 with media) and implanted in the flanks of Nude mice. When tumors reached ∼100mm 3 , mice were split into two cohorts and treatment was started. For (A-C), tumors were treated with vehicle (20% DMSO in saline) or YM155 (20 μM) via intratumoral injection twice a week (vehicle n=5, YM155 n=6). For (D-F), mice were treated with vehicle (saline) or YM155 (10 mg/kg/day) via micro-osmotic pump (vehicle n=6, YM155 n=5). Caliper measurements were made twice a week to monitor tumor growth (A,D) and resulting tumors were collected, photographed (B,E), and weighed (C,F). Experiments were repeated 2 (A-C) and 3 times (D-F) respectively. Both intra-tumoral and systemic treatment with YM155 decreased tumor size over time compared to vehicle control. (p

    Journal: Oncogene

    Article Title: Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma

    doi: 10.1038/onc.2014.304

    Figure Lengend Snippet: YM155 inhibits growth of Ptch mutant tumor cells in vivo (A-F) Tumor cells were suspended in GFR matrigel (1:1 with media) and implanted in the flanks of Nude mice. When tumors reached ∼100mm 3 , mice were split into two cohorts and treatment was started. For (A-C), tumors were treated with vehicle (20% DMSO in saline) or YM155 (20 μM) via intratumoral injection twice a week (vehicle n=5, YM155 n=6). For (D-F), mice were treated with vehicle (saline) or YM155 (10 mg/kg/day) via micro-osmotic pump (vehicle n=6, YM155 n=5). Caliper measurements were made twice a week to monitor tumor growth (A,D) and resulting tumors were collected, photographed (B,E), and weighed (C,F). Experiments were repeated 2 (A-C) and 3 times (D-F) respectively. Both intra-tumoral and systemic treatment with YM155 decreased tumor size over time compared to vehicle control. (p

    Article Snippet: To evaluate Survivin expression after YM155 treatment, tumor cells were plated on 6-well plates (6-8M cells/well) and treated with YM155 or DMSO (Fisher Scientific Inc. San Diego, CA) at 1 μM for 24hrs and processed as described above.

    Techniques: Mutagenesis, In Vivo, Mouse Assay, Injection

    Survivin antagonists inhibit proliferation (A-D) Tumor cells were plated on chamber slides and treated for 24 hr with control media (A), 0.1% DMSO (B), 10 μg/ml S12 (C), or 50 nM YM155 (D). Cells were stained with anti-Ki67 antibodies (green) to mark proliferating cells and DAPI (blue) to label cell nuclei. Very few cells were Ki67+ after treatment with Survivin antagonists compared to controls (p

    Journal: Oncogene

    Article Title: Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma

    doi: 10.1038/onc.2014.304

    Figure Lengend Snippet: Survivin antagonists inhibit proliferation (A-D) Tumor cells were plated on chamber slides and treated for 24 hr with control media (A), 0.1% DMSO (B), 10 μg/ml S12 (C), or 50 nM YM155 (D). Cells were stained with anti-Ki67 antibodies (green) to mark proliferating cells and DAPI (blue) to label cell nuclei. Very few cells were Ki67+ after treatment with Survivin antagonists compared to controls (p

    Article Snippet: To evaluate Survivin expression after YM155 treatment, tumor cells were plated on 6-well plates (6-8M cells/well) and treated with YM155 or DMSO (Fisher Scientific Inc. San Diego, CA) at 1 μM for 24hrs and processed as described above.

    Techniques: Staining

    Survivin antagonists alter cell cycle progression and promote apoptosis (A-H) Ptch mutant tumor cells were treated with either DMSO (A,B,E,F), 20 μg/ml S12 (C,D), or 100 nM YM155 (G,H) and stained with 7-AAD for cell cycle analysis after 24 hr (A,C,E,G) or 36 hr (B,D,F,H). YM155 decreased the percentage of cells in G2/M, while S12 treatment caused an accumulation of cells in G2/M. Data represent 4 (A-D) and 6 (E-H) experiments and percentages based on live cell gates (excluded subG1). (I-K) Tumor cells were treated with DMSO (I), 20 μg/ml (J), or 100nM YM155 (K) for 36 hr, then collected and stained with Propidium Iodide (PI) and Annexin-V for FACS analysis. The percentage of apoptotic cells was significantly higher after antagonist treatment compared to control. Data represent 6 independent experiments.

    Journal: Oncogene

    Article Title: Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma

    doi: 10.1038/onc.2014.304

    Figure Lengend Snippet: Survivin antagonists alter cell cycle progression and promote apoptosis (A-H) Ptch mutant tumor cells were treated with either DMSO (A,B,E,F), 20 μg/ml S12 (C,D), or 100 nM YM155 (G,H) and stained with 7-AAD for cell cycle analysis after 24 hr (A,C,E,G) or 36 hr (B,D,F,H). YM155 decreased the percentage of cells in G2/M, while S12 treatment caused an accumulation of cells in G2/M. Data represent 4 (A-D) and 6 (E-H) experiments and percentages based on live cell gates (excluded subG1). (I-K) Tumor cells were treated with DMSO (I), 20 μg/ml (J), or 100nM YM155 (K) for 36 hr, then collected and stained with Propidium Iodide (PI) and Annexin-V for FACS analysis. The percentage of apoptotic cells was significantly higher after antagonist treatment compared to control. Data represent 6 independent experiments.

    Article Snippet: To evaluate Survivin expression after YM155 treatment, tumor cells were plated on 6-well plates (6-8M cells/well) and treated with YM155 or DMSO (Fisher Scientific Inc. San Diego, CA) at 1 μM for 24hrs and processed as described above.

    Techniques: Mutagenesis, Staining, Cell Cycle Assay, FACS

    Survivin antagonists inhibit proliferation of human SHH-driven MB cells Cells isolated from LDE225-sensitive xenograft DMB012 (A) and LDE-insensitive xenografts RCMB018 (B) and ICb-984MB (C) were treated for 48 hr with DMSO, LDE225, YM155 or S12, and analyzed for thymidine incorporation following a 12-16 hr pulse. All tumor cells were sensitive to YM155 inhibition and high dose S12 treatment (DMB012 p

    Journal: Oncogene

    Article Title: Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma

    doi: 10.1038/onc.2014.304

    Figure Lengend Snippet: Survivin antagonists inhibit proliferation of human SHH-driven MB cells Cells isolated from LDE225-sensitive xenograft DMB012 (A) and LDE-insensitive xenografts RCMB018 (B) and ICb-984MB (C) were treated for 48 hr with DMSO, LDE225, YM155 or S12, and analyzed for thymidine incorporation following a 12-16 hr pulse. All tumor cells were sensitive to YM155 inhibition and high dose S12 treatment (DMB012 p

    Article Snippet: To evaluate Survivin expression after YM155 treatment, tumor cells were plated on 6-well plates (6-8M cells/well) and treated with YM155 or DMSO (Fisher Scientific Inc. San Diego, CA) at 1 μM for 24hrs and processed as described above.

    Techniques: Isolation, Inhibition

    HSulf-1 in combination with palbociclib exerts synergistic antitumor effects by inducing G 1 /S stage cell cycle arrest and by inhibiting migration, invasion and epithelial-mesenchymal transition in vitro . (A-E) Hs578T and MDA-MB-231 cells following transient transfection with the control vector or HSulf-1 overexpression plasmids and incubation with 500 nM palbociclib or DMSO for 72 h. (A) Cell cycle analysis. G 1 and S phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-Vector+Palbociclib; G 1 and G 2 phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-HSulf-1+Vehicle; G 1 phase of pcDNA3.0-Vector+Palbociclib vs. pcDNA3.0-HSulf-1+Palbociclib; G 1 phase of pcDNA3.0-HSulf-1+Vehicle vs. pcDNA3.0-HSulf-1+Palbociclib. (B) Apoptosis analysis. (C) Wound healing assays. (D) Transwell assays. Magnification, x100. (E) Western blotting was performed to measure E-cadherin, vimentin and N-cadherin expression, with β-actin used as an internal control. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Journal: International Journal of Oncology

    Article Title: HSulf-1 and palbociclib exert synergistic antitumor effects on RB-positive triple-negative breast cancer

    doi: 10.3892/ijo.2020.5057

    Figure Lengend Snippet: HSulf-1 in combination with palbociclib exerts synergistic antitumor effects by inducing G 1 /S stage cell cycle arrest and by inhibiting migration, invasion and epithelial-mesenchymal transition in vitro . (A-E) Hs578T and MDA-MB-231 cells following transient transfection with the control vector or HSulf-1 overexpression plasmids and incubation with 500 nM palbociclib or DMSO for 72 h. (A) Cell cycle analysis. G 1 and S phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-Vector+Palbociclib; G 1 and G 2 phases of pcDNA3.0-Vector+Vehicle vs. pcDNA3.0-HSulf-1+Vehicle; G 1 phase of pcDNA3.0-Vector+Palbociclib vs. pcDNA3.0-HSulf-1+Palbociclib; G 1 phase of pcDNA3.0-HSulf-1+Vehicle vs. pcDNA3.0-HSulf-1+Palbociclib. (B) Apoptosis analysis. (C) Wound healing assays. (D) Transwell assays. Magnification, x100. (E) Western blotting was performed to measure E-cadherin, vimentin and N-cadherin expression, with β-actin used as an internal control. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Article Snippet: Palbociclib (Sigma-Aldrich; Merck KGaA) was dissolved in DMSO, following which the cells were treated with 500 nM palboci-clib for 72 h at 37°C.

    Techniques: Migration, In Vitro, Multiple Displacement Amplification, Transfection, Plasmid Preparation, Over Expression, Incubation, Cell Cycle Assay, Western Blot, Expressing, Derivative Assay

    HSulf-1 exhibit synergy with palbociclib to exert antiproliferative effects on breast cancer cells by reducing palbociclib-induced cyclin D1 accumulation. (A) Western blotting was performed to measure the protein levels of cyclin D1, p-RB and total RB in Hs578T and MDA-MB-231 cells following transient transfection with the control vector or HSulf-1 overexpression plasmids and incubation with 500 nM palbociclib or DMSO. β-Actin was used as an internal control. (B) Reverse transcription-quantitative PCR was performed to measure mRNA level of cyclin D1 in MDA-MB-231 cells following transient transfection with the control vector or cyclin D1 overexpression plasmids. GAPDH was used as an internal control. (C) Cell Counting Kit-8 and (D) colony formation assays were performed to evaluate cell viability in MDA-MB-231 cells following incubation with 500 nM palbociclib for 14 days, overexpression of HSulf-1, overexpression of HSulf-1 followed by incubation with 500 nM palbociclib for 14 days or co-transfection of plasmids encoding HSulf-1 and cyclin D1 followed by exposure to palbociclib for 14 days. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Journal: International Journal of Oncology

    Article Title: HSulf-1 and palbociclib exert synergistic antitumor effects on RB-positive triple-negative breast cancer

    doi: 10.3892/ijo.2020.5057

    Figure Lengend Snippet: HSulf-1 exhibit synergy with palbociclib to exert antiproliferative effects on breast cancer cells by reducing palbociclib-induced cyclin D1 accumulation. (A) Western blotting was performed to measure the protein levels of cyclin D1, p-RB and total RB in Hs578T and MDA-MB-231 cells following transient transfection with the control vector or HSulf-1 overexpression plasmids and incubation with 500 nM palbociclib or DMSO. β-Actin was used as an internal control. (B) Reverse transcription-quantitative PCR was performed to measure mRNA level of cyclin D1 in MDA-MB-231 cells following transient transfection with the control vector or cyclin D1 overexpression plasmids. GAPDH was used as an internal control. (C) Cell Counting Kit-8 and (D) colony formation assays were performed to evaluate cell viability in MDA-MB-231 cells following incubation with 500 nM palbociclib for 14 days, overexpression of HSulf-1, overexpression of HSulf-1 followed by incubation with 500 nM palbociclib for 14 days or co-transfection of plasmids encoding HSulf-1 and cyclin D1 followed by exposure to palbociclib for 14 days. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Article Snippet: Palbociclib (Sigma-Aldrich; Merck KGaA) was dissolved in DMSO, following which the cells were treated with 500 nM palboci-clib for 72 h at 37°C.

    Techniques: Western Blot, Multiple Displacement Amplification, Transfection, Plasmid Preparation, Over Expression, Incubation, Real-time Polymerase Chain Reaction, Cell Counting, Cotransfection, Derivative Assay

    HSulf-1 inhibits cell proliferation and when combined with palbociclib, exerts antiproliferative effects on RB-positive TNBC cells in a synergistic manner both in vitro and in vivo . (A) Hs578T and MDA-MB-231 cells were transiently transfected with the control vector or HSulf-1 overexpression plasmids and incubated for 6 h at 37°C then incubated with fresh complete medium cantaining 500 nM palbociclib or DMSO for 0, 24, 48 and 72 h. Subsequently, Cell Counting Kit-8 assays were performed to assess cell viability. (B) Hs578T and MDA-MB-231 cells were transiently transfected with the control vector or HSulf-1 overexpression plasmids and incubated for 6 h at 37°C then incubated with fresh complete medium containing 500 nM palbociclib or DMSO for up to 14 days for colony formation assay. (C) Representative images of the mouse xenograft models and tumors extracted from the four treatment groups after euthanasia. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Journal: International Journal of Oncology

    Article Title: HSulf-1 and palbociclib exert synergistic antitumor effects on RB-positive triple-negative breast cancer

    doi: 10.3892/ijo.2020.5057

    Figure Lengend Snippet: HSulf-1 inhibits cell proliferation and when combined with palbociclib, exerts antiproliferative effects on RB-positive TNBC cells in a synergistic manner both in vitro and in vivo . (A) Hs578T and MDA-MB-231 cells were transiently transfected with the control vector or HSulf-1 overexpression plasmids and incubated for 6 h at 37°C then incubated with fresh complete medium cantaining 500 nM palbociclib or DMSO for 0, 24, 48 and 72 h. Subsequently, Cell Counting Kit-8 assays were performed to assess cell viability. (B) Hs578T and MDA-MB-231 cells were transiently transfected with the control vector or HSulf-1 overexpression plasmids and incubated for 6 h at 37°C then incubated with fresh complete medium containing 500 nM palbociclib or DMSO for up to 14 days for colony formation assay. (C) Representative images of the mouse xenograft models and tumors extracted from the four treatment groups after euthanasia. The results were derived from three independent experiments. Data are presented as the mean ± SD. * P

    Article Snippet: Palbociclib (Sigma-Aldrich; Merck KGaA) was dissolved in DMSO, following which the cells were treated with 500 nM palboci-clib for 72 h at 37°C.

    Techniques: In Vitro, In Vivo, Multiple Displacement Amplification, Transfection, Plasmid Preparation, Over Expression, Incubation, Cell Counting, Colony Assay, Derivative Assay

    In vivo activity of EN4 in a mouse tissue cage model. The numbers of planktonic SA113 (A) and the viability of leukocytes (B) present in tissue cage fluid from cages treated with 100 or 250 μg of EN4 or 30 μg of daptomycin (DAP) and infected with 4 × 10 3 CFU of SA113 were investigated. Open circles indicate control mice injected with 1% DMSO-PBS. The values shown are means ± the SDs.

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Antimicrobial Properties of 8-Hydroxyserrulat-14-en-19-oic Acid for Treatment of Implant-Associated Infections

    doi: 10.1128/AAC.01735-12

    Figure Lengend Snippet: In vivo activity of EN4 in a mouse tissue cage model. The numbers of planktonic SA113 (A) and the viability of leukocytes (B) present in tissue cage fluid from cages treated with 100 or 250 μg of EN4 or 30 μg of daptomycin (DAP) and infected with 4 × 10 3 CFU of SA113 were investigated. Open circles indicate control mice injected with 1% DMSO-PBS. The values shown are means ± the SDs.

    Article Snippet: EN4 was dissolved in 1% dimethyl sulfoxide (DMSO) (Merck, Darmstadt, Germany) in phosphate-buffered saline (PBS) (Reagens, Basel, Switzerland) (DMSO-PBS) up to a concentration of 400 μg/ml.

    Techniques: In Vivo, Activity Assay, Infection, Mouse Assay, Injection

    Effect of EN4 on bacterial membrane integrity. (A) S. epidermidis 1457 was incubated for 10 min with EN4 or CHX at 100 μg/ml or 1% DMSO-PBS and subsequently double stained with propidium iodide (PI) and SYTO9 and analyzed by flow cytometry. The results of one representative experiment of three performed are shown. (B) Transmission electron microscopy images of ultrathin sections of WSPPA treated for 1 h with 1% DMSO-PBS as a control, EN4 at 100 or 200 μg/ml, or 250 μg of CHX/ml. Arrowheads indicate ultrastructural changes; the bars represent 200 nm. (C) WSPPA was treated for 10 min with EN4 or CHX at 100 μg/ml, followed by centrifugation and investigation of supernatants for the presence of ATP using luciferase reaction. Nisin (NIS) and ciprofloxacin (CIP) were used as a positive and a negative control, respectively, and 1% DMSO-PBS was used as an untreated control (Ctrl). The values shown are means ± the SDs of areas under the concentration-time curve calculated for the first 30 min of luciferase reaction from at least three independent experiments prepared in duplicates. Significant ATP leakage compared to results for the untreated control is indicated (*, P

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Antimicrobial Properties of 8-Hydroxyserrulat-14-en-19-oic Acid for Treatment of Implant-Associated Infections

    doi: 10.1128/AAC.01735-12

    Figure Lengend Snippet: Effect of EN4 on bacterial membrane integrity. (A) S. epidermidis 1457 was incubated for 10 min with EN4 or CHX at 100 μg/ml or 1% DMSO-PBS and subsequently double stained with propidium iodide (PI) and SYTO9 and analyzed by flow cytometry. The results of one representative experiment of three performed are shown. (B) Transmission electron microscopy images of ultrathin sections of WSPPA treated for 1 h with 1% DMSO-PBS as a control, EN4 at 100 or 200 μg/ml, or 250 μg of CHX/ml. Arrowheads indicate ultrastructural changes; the bars represent 200 nm. (C) WSPPA was treated for 10 min with EN4 or CHX at 100 μg/ml, followed by centrifugation and investigation of supernatants for the presence of ATP using luciferase reaction. Nisin (NIS) and ciprofloxacin (CIP) were used as a positive and a negative control, respectively, and 1% DMSO-PBS was used as an untreated control (Ctrl). The values shown are means ± the SDs of areas under the concentration-time curve calculated for the first 30 min of luciferase reaction from at least three independent experiments prepared in duplicates. Significant ATP leakage compared to results for the untreated control is indicated (*, P

    Article Snippet: EN4 was dissolved in 1% dimethyl sulfoxide (DMSO) (Merck, Darmstadt, Germany) in phosphate-buffered saline (PBS) (Reagens, Basel, Switzerland) (DMSO-PBS) up to a concentration of 400 μg/ml.

    Techniques: Incubation, Staining, Flow Cytometry, Cytometry, Transmission Assay, Electron Microscopy, Centrifugation, Luciferase, Negative Control, Concentration Assay

    Analogs of honokiol do not bind or inhibit FOXM1 a C3-luc cells were induced with doxycycline and treated with the indicated analogs of honokiol at the concentration of 40 µM for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b DU145 prostate cancer cells were treated as indicated. Following treatment cells were collected and immunoblotting was performed for FOXM1, cleaved caspase-3 and β-actin as the loading control. c STD NMR spectra of 2 mM of: (I) 2 mM eugenol, (II) 2 mM O -eugenol, (III) 2 mM 2-allylphenol and (IV) 2 mM 2,2 dihydroxybiphenyl. The chemical structure of each small molecule is illustrated. Signals from vehicle (DMSO) and water are labeled. d STD NMR spectra of 150 ng of recombinant FOXM1 plus: (I) 2 mM eugenol, (II) 2 mM O-eugenol, (III) 2 mM 2,2 dihydroxybiphenyl and (IV) 2 mM 2-allylphenol. The chemical structure of each small molecule is illustrated. STD signals arising from the aryl groups are annotated and signals from vehicle (DMSO) and water are labeled

    Journal: Cell Death & Disease

    Article Title: Honokiol is a FOXM1 antagonist

    doi: 10.1038/s41419-017-0156-7

    Figure Lengend Snippet: Analogs of honokiol do not bind or inhibit FOXM1 a C3-luc cells were induced with doxycycline and treated with the indicated analogs of honokiol at the concentration of 40 µM for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b DU145 prostate cancer cells were treated as indicated. Following treatment cells were collected and immunoblotting was performed for FOXM1, cleaved caspase-3 and β-actin as the loading control. c STD NMR spectra of 2 mM of: (I) 2 mM eugenol, (II) 2 mM O -eugenol, (III) 2 mM 2-allylphenol and (IV) 2 mM 2,2 dihydroxybiphenyl. The chemical structure of each small molecule is illustrated. Signals from vehicle (DMSO) and water are labeled. d STD NMR spectra of 150 ng of recombinant FOXM1 plus: (I) 2 mM eugenol, (II) 2 mM O-eugenol, (III) 2 mM 2,2 dihydroxybiphenyl and (IV) 2 mM 2-allylphenol. The chemical structure of each small molecule is illustrated. STD signals arising from the aryl groups are annotated and signals from vehicle (DMSO) and water are labeled

    Article Snippet: MG132 (EMD Millipore), thiostrepton (Sigma), honokiol, 2,2 dihydroxybiphenyl, 2 allylphenol, eugenol, and O -eugenol were dissolved in dimethyl sulfoxide (DMSO) (Fisher Scientific), N-acetyl-l-cysteine (NAC) (Sigma) in deionized water, and doxycycline (LKT Laboratories) in phosphate buffered saline (PBS).

    Techniques: Concentration Assay, Luciferase, Activity Assay, Nuclear Magnetic Resonance, Labeling, Recombinant

    Honokiol inhibits FOXM1 transactivation via binding a C3-luc cells were induced with doxycycline and treated with honokiol for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b The C3 cell line was treated with doxycycline and honokiol in the indicated concentrations for 24 h. Cells were collected and immunoblotting was performed with a FOXM1 specific antibody. β-actin was used as the loading control. c Representative EMSA image shows the inhibitory effect of honokiol on the formation of the FOXM1 DBD protein–DNA complex. d The C3 cell line was treated with doxycycline and honokiol as indicated for 24 h. Then, cells were processed for the ChIP experiments, as described in “Materials and methods”. Graph shows mean ± SEM of two independent ChIP experiments. e Saturation transfer difference (STD) NMR spectra to assess the binding of honokiol to FOXM1: (I) 2 mM of honokiol alone, (II) 150 ng of recombinant FOXM1 alone, (III) 2 mM honokiol with 150 ng of recombinant FOXM1. The chemical structure of honokiol is illustrated. STD signals arising from the aryl groups in honokiol are annotated, and signals from vehicle (DMSO) and water are labeled

    Journal: Cell Death & Disease

    Article Title: Honokiol is a FOXM1 antagonist

    doi: 10.1038/s41419-017-0156-7

    Figure Lengend Snippet: Honokiol inhibits FOXM1 transactivation via binding a C3-luc cells were induced with doxycycline and treated with honokiol for 24 h. The luciferase activity was determined by using the Luciferase Assay System (Promega). Graph shows quantification as fold induction of firefly luciferase activity compared to control cells, mean ± SD of a representative triplicate experiment. b The C3 cell line was treated with doxycycline and honokiol in the indicated concentrations for 24 h. Cells were collected and immunoblotting was performed with a FOXM1 specific antibody. β-actin was used as the loading control. c Representative EMSA image shows the inhibitory effect of honokiol on the formation of the FOXM1 DBD protein–DNA complex. d The C3 cell line was treated with doxycycline and honokiol as indicated for 24 h. Then, cells were processed for the ChIP experiments, as described in “Materials and methods”. Graph shows mean ± SEM of two independent ChIP experiments. e Saturation transfer difference (STD) NMR spectra to assess the binding of honokiol to FOXM1: (I) 2 mM of honokiol alone, (II) 150 ng of recombinant FOXM1 alone, (III) 2 mM honokiol with 150 ng of recombinant FOXM1. The chemical structure of honokiol is illustrated. STD signals arising from the aryl groups in honokiol are annotated, and signals from vehicle (DMSO) and water are labeled

    Article Snippet: MG132 (EMD Millipore), thiostrepton (Sigma), honokiol, 2,2 dihydroxybiphenyl, 2 allylphenol, eugenol, and O -eugenol were dissolved in dimethyl sulfoxide (DMSO) (Fisher Scientific), N-acetyl-l-cysteine (NAC) (Sigma) in deionized water, and doxycycline (LKT Laboratories) in phosphate buffered saline (PBS).

    Techniques: Binding Assay, Luciferase, Activity Assay, Chromatin Immunoprecipitation, Nuclear Magnetic Resonance, Recombinant, Labeling

    Dose-dependent antifungal effect of L1 against Botrytis cinerea B05.10 at 4 °C. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Journal: Molecules

    Article Title: Structural Characterization, DFT Calculation, NCI, Scan-Rate Analysis and Antifungal Activity against Botrytis cinerea of (E)-2-{[(2-Aminopyridin-2-yl)imino]-methyl}-4,6-di-tert-butylphenol (Pyridine Schiff Base)

    doi: 10.3390/molecules25122741

    Figure Lengend Snippet: Dose-dependent antifungal effect of L1 against Botrytis cinerea B05.10 at 4 °C. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Article Snippet: To this end, Petri dishes (90 mm) with a final volume of 15 mL of PDA (Difco) containing 0 (negative control), 2, 4, 6, 8 or 10 ppm of L1 dissolved in DMSO (Merck) were used.

    Techniques: Inhibition, Concentration Assay

    Antifungal effect against Botrytis cinerea A1 (at 26 °C) exerted by L1 in a dose-dependent manner (12 days of incubation). Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (6 ppm) and compared with the commercial fungicide fenhexamid (6 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (0.045% v/v ). The figure shows a representative experiment, showing the fungal colony growth.

    Journal: Molecules

    Article Title: Structural Characterization, DFT Calculation, NCI, Scan-Rate Analysis and Antifungal Activity against Botrytis cinerea of (E)-2-{[(2-Aminopyridin-2-yl)imino]-methyl}-4,6-di-tert-butylphenol (Pyridine Schiff Base)

    doi: 10.3390/molecules25122741

    Figure Lengend Snippet: Antifungal effect against Botrytis cinerea A1 (at 26 °C) exerted by L1 in a dose-dependent manner (12 days of incubation). Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (6 ppm) and compared with the commercial fungicide fenhexamid (6 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (0.045% v/v ). The figure shows a representative experiment, showing the fungal colony growth.

    Article Snippet: To this end, Petri dishes (90 mm) with a final volume of 15 mL of PDA (Difco) containing 0 (negative control), 2, 4, 6, 8 or 10 ppm of L1 dissolved in DMSO (Merck) were used.

    Techniques: Incubation, Inhibition, Concentration Assay

    Dose-dependent antifungal effect of L1 against Botrytis cinerea A1 at 4 °C. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Journal: Molecules

    Article Title: Structural Characterization, DFT Calculation, NCI, Scan-Rate Analysis and Antifungal Activity against Botrytis cinerea of (E)-2-{[(2-Aminopyridin-2-yl)imino]-methyl}-4,6-di-tert-butylphenol (Pyridine Schiff Base)

    doi: 10.3390/molecules25122741

    Figure Lengend Snippet: Dose-dependent antifungal effect of L1 against Botrytis cinerea A1 at 4 °C. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Article Snippet: To this end, Petri dishes (90 mm) with a final volume of 15 mL of PDA (Difco) containing 0 (negative control), 2, 4, 6, 8 or 10 ppm of L1 dissolved in DMSO (Merck) were used.

    Techniques: Inhibition, Concentration Assay

    Antifungal effect against Botrytis cinerea A1 (at 26 °C) exerted by L1 in a dose-dependent manner. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Journal: Molecules

    Article Title: Structural Characterization, DFT Calculation, NCI, Scan-Rate Analysis and Antifungal Activity against Botrytis cinerea of (E)-2-{[(2-Aminopyridin-2-yl)imino]-methyl}-4,6-di-tert-butylphenol (Pyridine Schiff Base)

    doi: 10.3390/molecules25122741

    Figure Lengend Snippet: Antifungal effect against Botrytis cinerea A1 (at 26 °C) exerted by L1 in a dose-dependent manner. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Article Snippet: To this end, Petri dishes (90 mm) with a final volume of 15 mL of PDA (Difco) containing 0 (negative control), 2, 4, 6, 8 or 10 ppm of L1 dissolved in DMSO (Merck) were used.

    Techniques: Inhibition, Concentration Assay

    Antifungal effect against Botrytis cinerea B05.10 (at 26 °C) exerted by L1 in a dose-dependent manner. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Journal: Molecules

    Article Title: Structural Characterization, DFT Calculation, NCI, Scan-Rate Analysis and Antifungal Activity against Botrytis cinerea of (E)-2-{[(2-Aminopyridin-2-yl)imino]-methyl}-4,6-di-tert-butylphenol (Pyridine Schiff Base)

    doi: 10.3390/molecules25122741

    Figure Lengend Snippet: Antifungal effect against Botrytis cinerea B05.10 (at 26 °C) exerted by L1 in a dose-dependent manner. Inhibition of mycelial growth (by measuring the colony diameter) was observed in the presence of L1 (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm) and compared with the commercial fungicide fenhexamid (( A ): 0 ppm, ( B ): 2 ppm, ( C ): 4 ppm, ( D ): 6 ppm, ( E ): 8 ppm, ( F ): 10 ppm). Since both L1 and fenhexamid stock were dissolved in DMSO (vehicle), DMSO alone was also tested, adding the same concentration used with either L1 or fenhexamid in each case (( A ): 0% v/v , ( B ): 0.015% v/v , ( C ): 0.030% v/v , ( D ): 0.045% v/v , ( E ): 0.060% v/v , ( F ): 0.075% v/v ) (DMSO [eq]). In all cases, the experiments were performed in biological triplicate.

    Article Snippet: To this end, Petri dishes (90 mm) with a final volume of 15 mL of PDA (Difco) containing 0 (negative control), 2, 4, 6, 8 or 10 ppm of L1 dissolved in DMSO (Merck) were used.

    Techniques: Inhibition, Concentration Assay

    DWORF activates SERCA2a in the absence of PLB. (A) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). (B) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF-P15/W22 (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). GFP-SERCA2a was stably expressed in HEK293 cells, then 20 μg of DNA per dish (for unlabeled DWORF or unlabeled mutant DWORF) was transiently transfected into the cells. Ca-ATPase assays were performed using cell homogenates as described in Methods. Activity was normalized to the control (SERCA2a only), since DWORF had no significant effect on V max . (n=3)

    Journal: bioRxiv

    Article Title: The transmembrane domain of DWORF activates SERCA directly; P15 and W22 residues are essential

    doi: 10.1101/2020.09.18.303644

    Figure Lengend Snippet: DWORF activates SERCA2a in the absence of PLB. (A) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). (B) Ca-ATPase activity measured in homogenates of cells expressing GFP-SERCA2a and unlabeled DWORF-P15/W22 (black, pK Ca = 6.36 ± 0.04) or GFP-SERCA2a only (red, pK Ca = 6.08 ± 0.03). GFP-SERCA2a was stably expressed in HEK293 cells, then 20 μg of DNA per dish (for unlabeled DWORF or unlabeled mutant DWORF) was transiently transfected into the cells. Ca-ATPase assays were performed using cell homogenates as described in Methods. Activity was normalized to the control (SERCA2a only), since DWORF had no significant effect on V max . (n=3)

    Article Snippet: 24 hours before transfection, HEK293 cells were plated at 0.4 million cells per well in 6-well plates, or 2 million cells per dish in 10-centimeter dishes.

    Techniques: Activity Assay, Expressing, Stable Transfection, Mutagenesis, Transfection

    FRET-detected interaction of SERCA with the isolated TM domain of DWORF is similar to that with full-length DWORF. (A) FRET efficiency (E) in HEK293 cells stably expressing GFP-SERCA2a, vs. μg/dish of DNA transiently transfected into HEK293 cells expressing RFP-TM-DWORF (black) or full-length RFP-DWORF (red). (B) Fraction X DA of donors (GFP) transferring energy (bound) to acceptor (RFP) determined for samples in panel A. (C) FRET efficiency E for increasing amounts of TM-DWORF DNA transfected into a stable cell line expressing GFP-SERCA2a and RFP-PLB. (D) FRET efficiency plotted vs. DNA transfected per well. D. Fraction X DA of donors transferring energy (bound) to acceptors determined for samples in C.

    Journal: bioRxiv

    Article Title: The transmembrane domain of DWORF activates SERCA directly; P15 and W22 residues are essential

    doi: 10.1101/2020.09.18.303644

    Figure Lengend Snippet: FRET-detected interaction of SERCA with the isolated TM domain of DWORF is similar to that with full-length DWORF. (A) FRET efficiency (E) in HEK293 cells stably expressing GFP-SERCA2a, vs. μg/dish of DNA transiently transfected into HEK293 cells expressing RFP-TM-DWORF (black) or full-length RFP-DWORF (red). (B) Fraction X DA of donors (GFP) transferring energy (bound) to acceptor (RFP) determined for samples in panel A. (C) FRET efficiency E for increasing amounts of TM-DWORF DNA transfected into a stable cell line expressing GFP-SERCA2a and RFP-PLB. (D) FRET efficiency plotted vs. DNA transfected per well. D. Fraction X DA of donors transferring energy (bound) to acceptors determined for samples in C.

    Article Snippet: 24 hours before transfection, HEK293 cells were plated at 0.4 million cells per well in 6-well plates, or 2 million cells per dish in 10-centimeter dishes.

    Techniques: Isolation, Stable Transfection, Expressing, Transfection, Transferring

    RFP-DWORF binding to GFP-SERCA2a in live cells. (A) Confocal microscopy images of GFP-SERCA (donor) and RFP-DWORF (acceptor) fluorescence signals. (B) Fluorescence lifetime (FLT) traces measured from HEK293 cells stably expressing the donor without (green, F D (t) or with (red, F D+A (t)) transient expression of the acceptor. FLT data was analyzed as described in Methods to determine lifetimes (τ D and τ D+A ) and mole fractions X D and X DA . (C) FRET efficiency E (1-τ D+A /τ D ) vs. μg of acceptor DNA seeded per dish. (D) The fraction of SERCA2a containing bound DWORF (X DA ).

    Journal: bioRxiv

    Article Title: The transmembrane domain of DWORF activates SERCA directly; P15 and W22 residues are essential

    doi: 10.1101/2020.09.18.303644

    Figure Lengend Snippet: RFP-DWORF binding to GFP-SERCA2a in live cells. (A) Confocal microscopy images of GFP-SERCA (donor) and RFP-DWORF (acceptor) fluorescence signals. (B) Fluorescence lifetime (FLT) traces measured from HEK293 cells stably expressing the donor without (green, F D (t) or with (red, F D+A (t)) transient expression of the acceptor. FLT data was analyzed as described in Methods to determine lifetimes (τ D and τ D+A ) and mole fractions X D and X DA . (C) FRET efficiency E (1-τ D+A /τ D ) vs. μg of acceptor DNA seeded per dish. (D) The fraction of SERCA2a containing bound DWORF (X DA ).

    Article Snippet: 24 hours before transfection, HEK293 cells were plated at 0.4 million cells per well in 6-well plates, or 2 million cells per dish in 10-centimeter dishes.

    Techniques: Binding Assay, Confocal Microscopy, Fluorescence, Stable Transfection, Expressing

    RFP-DWORF activates SERCA2a directly in the absence of PLB. Transient transfections of 5μg of RFP-DWORF into HEK293 cells stably expressing GFP-SERCA2a. 48 hours after transfection, cells was harvested at 10 million per mL in homogenization buffer (0.5mM MgCl2, 10mM Tris-HCL ph 7.5, DNase I and protease inhibitor). Cells was then lysed by Tissumizer (Tekmar SDT-1810) and prepared in 96well plate for ATPase assay. n=3

    Journal: bioRxiv

    Article Title: The transmembrane domain of DWORF activates SERCA directly; P15 and W22 residues are essential

    doi: 10.1101/2020.09.18.303644

    Figure Lengend Snippet: RFP-DWORF activates SERCA2a directly in the absence of PLB. Transient transfections of 5μg of RFP-DWORF into HEK293 cells stably expressing GFP-SERCA2a. 48 hours after transfection, cells was harvested at 10 million per mL in homogenization buffer (0.5mM MgCl2, 10mM Tris-HCL ph 7.5, DNase I and protease inhibitor). Cells was then lysed by Tissumizer (Tekmar SDT-1810) and prepared in 96well plate for ATPase assay. n=3

    Article Snippet: 24 hours before transfection, HEK293 cells were plated at 0.4 million cells per well in 6-well plates, or 2 million cells per dish in 10-centimeter dishes.

    Techniques: Transfection, Stable Transfection, Expressing, Homogenization, Protease Inhibitor, ATPase Assay

    TM-DWORF can activate SERCA2a directly in the absence of PLB. Transient transfections of 5μg of TM-DWORF into HEK293 cells stably expressing GFP-SERCA2a. 48 hours after transfection, cells was harvested at 10 million per mL in homogenization buffer (0.5mM MgCl2, 10mM Tris-HCL ph 7.5, DNase I and protease inhibitor). Cells was then lysed by Tissumizer (Tekmar SDT-1810) and prepared in 96well plate for ATPase assay. n=3

    Journal: bioRxiv

    Article Title: The transmembrane domain of DWORF activates SERCA directly; P15 and W22 residues are essential

    doi: 10.1101/2020.09.18.303644

    Figure Lengend Snippet: TM-DWORF can activate SERCA2a directly in the absence of PLB. Transient transfections of 5μg of TM-DWORF into HEK293 cells stably expressing GFP-SERCA2a. 48 hours after transfection, cells was harvested at 10 million per mL in homogenization buffer (0.5mM MgCl2, 10mM Tris-HCL ph 7.5, DNase I and protease inhibitor). Cells was then lysed by Tissumizer (Tekmar SDT-1810) and prepared in 96well plate for ATPase assay. n=3

    Article Snippet: 24 hours before transfection, HEK293 cells were plated at 0.4 million cells per well in 6-well plates, or 2 million cells per dish in 10-centimeter dishes.

    Techniques: Transfection, Stable Transfection, Expressing, Homogenization, Protease Inhibitor, ATPase Assay

    Treatment with HIT and SAHA results in a reduced proliferation in osteosarcoma xenografts. Histological analysis of proliferation in tumors treated with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The proliferation rate was significantly reduced in tumors after treatment with SAHA and HIT at all investigation time points. HIT only treatment led to a significantly lower proliferation rate 8 and 24 days after irradiation compared to the control group. SAHA only treatment had no significant effect on tumor proliferation

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: Treatment with HIT and SAHA results in a reduced proliferation in osteosarcoma xenografts. Histological analysis of proliferation in tumors treated with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The proliferation rate was significantly reduced in tumors after treatment with SAHA and HIT at all investigation time points. HIT only treatment led to a significantly lower proliferation rate 8 and 24 days after irradiation compared to the control group. SAHA only treatment had no significant effect on tumor proliferation

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Irradiation

    Density of microvessels is significantly reduced in osteosarcoma after combination treatment. Xenografts were treated with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The density of microvessels was reduced in tumors of all treatment groups at all investigation time points. Tumors treated with HIT and SAHA showed a significant (*) lower vascularization compared to tumors treated with HIT from day 24 on and the lowest vascularization at all

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: Density of microvessels is significantly reduced in osteosarcoma after combination treatment. Xenografts were treated with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The density of microvessels was reduced in tumors of all treatment groups at all investigation time points. Tumors treated with HIT and SAHA showed a significant (*) lower vascularization compared to tumors treated with HIT from day 24 on and the lowest vascularization at all

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Irradiation

    Impairment of apoptosis and necrosis after HIT and SAHA treatment. Apoptosis and necrosis in osteosarcoma xenografts were analyzed after treatment with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The combination treatment lead to a significant (*) induction of apoptosis one day, 8 and 45 days after HIT compared to HIT only treatment. Apoptosis was also increased after SAHA only and HIT only 24 h, 8 and 45 days after irradiation but not as much as treatment with HIT and SAHA. Combination of HIT and SAHA lead to a significant (*) induction of necrosis on day 45. SAHA only and HIT only treatment resulted in a significantly higher rate of necrosis from day 24 on but not at earlier time points compared to the control groups

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: Impairment of apoptosis and necrosis after HIT and SAHA treatment. Apoptosis and necrosis in osteosarcoma xenografts were analyzed after treatment with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. The combination treatment lead to a significant (*) induction of apoptosis one day, 8 and 45 days after HIT compared to HIT only treatment. Apoptosis was also increased after SAHA only and HIT only 24 h, 8 and 45 days after irradiation but not as much as treatment with HIT and SAHA. Combination of HIT and SAHA lead to a significant (*) induction of necrosis on day 45. SAHA only and HIT only treatment resulted in a significantly higher rate of necrosis from day 24 on but not at earlier time points compared to the control groups

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Irradiation

    Expression of p53 and p21 WAF1/CIP1 is impaired in osteosarcoma xenografts after treatment with HIT and SAHA. Expression of p53 and p21 WAF1/CIP1 was analyzed after treatment with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. p53 expression was increased in all SAHA treated tumors compared to the vehicle treated control and only irradiated tumors on day 23 and 45. Increased p21 Waf1/Cip1 expression was detected in tumors after SAHA only and SAHA and HIT treatment compared to the controls and the HIT treated tumors on day 8

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: Expression of p53 and p21 WAF1/CIP1 is impaired in osteosarcoma xenografts after treatment with HIT and SAHA. Expression of p53 and p21 WAF1/CIP1 was analyzed after treatment with DMSO (control), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or HIT and SAHA. p53 expression was increased in all SAHA treated tumors compared to the vehicle treated control and only irradiated tumors on day 23 and 45. Increased p21 Waf1/Cip1 expression was detected in tumors after SAHA only and SAHA and HIT treatment compared to the controls and the HIT treated tumors on day 8

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Expressing, Irradiation

    Combination of HIT and SAHA induces an increased local control. Tumor growth of osteosarcoma xenografts was determined after treatment with DMSO (controls), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or SAHA plus HIT. Local control was defined as tumor growth > 1000 m 3 and calculated according to the method of Kaplan and Meier. The combination of HIT and SAHA led to a significant local control compared to SAHA only and HIT only starting day

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: Combination of HIT and SAHA induces an increased local control. Tumor growth of osteosarcoma xenografts was determined after treatment with DMSO (controls), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or SAHA plus HIT. Local control was defined as tumor growth > 1000 m 3 and calculated according to the method of Kaplan and Meier. The combination of HIT and SAHA led to a significant local control compared to SAHA only and HIT only starting day

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Irradiation

    The combination of HIT and SAHA results in a significant tumor growth delay compared to treatment with HIT or SAHA only. Osteosarcoma xenografts were treated with DMSO (controls), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or SAHA plus HIT and tumor growth was determined until day 45 after HIT. Comparing HIT as mono-treatment to SAHA only, HIT seemed to be superior from day 10 on after treatment start reaching significance at day 23. The combination of HIT and SAHA yielded a significant (*) tumor growth retardation compared to SAHA only and HIT only starting day 20 and day 25 respectively

    Journal: Radiation Oncology (London, England)

    Article Title: Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy

    doi: 10.1186/s13014-015-0455-z

    Figure Lengend Snippet: The combination of HIT and SAHA results in a significant tumor growth delay compared to treatment with HIT or SAHA only. Osteosarcoma xenografts were treated with DMSO (controls), suberoylanilide hydroxamic acid (SAHA), irradiation (HIT) or SAHA plus HIT and tumor growth was determined until day 45 after HIT. Comparing HIT as mono-treatment to SAHA only, HIT seemed to be superior from day 10 on after treatment start reaching significance at day 23. The combination of HIT and SAHA yielded a significant (*) tumor growth retardation compared to SAHA only and HIT only starting day 20 and day 25 respectively

    Article Snippet: SAHA was obtained from Alexis Biochemicals (Lörrach, Germany), DMSO from Carl Roth Biochemicals (Karlsruhe, Germany).

    Techniques: Irradiation

    Gimatecan Inhibited HCC Cell Growth in Vitro . Different HCC cell lines were cultured and incubated with various concentrations of gimatecan at 37 ºC for 72 hours. The percentages of viable cells were measured at the end the incubation period. 100% refers to the number of cells after 72 hours of incubation in the presence of the vehicle control (0.1% DMSO).

    Journal: Asian Pacific Journal of Cancer Prevention : APJCP

    Article Title: In Vitro and In Vivo Anticancer Activity of Gimatecan against Hepatocellular Carcinoma

    doi: 10.22034/APJCP.2016.17.11.4853

    Figure Lengend Snippet: Gimatecan Inhibited HCC Cell Growth in Vitro . Different HCC cell lines were cultured and incubated with various concentrations of gimatecan at 37 ºC for 72 hours. The percentages of viable cells were measured at the end the incubation period. 100% refers to the number of cells after 72 hours of incubation in the presence of the vehicle control (0.1% DMSO).

    Article Snippet: Stock solutions of gimatecan were dissolved in 100% DMSO (Amresco, USA) and stored in sterilized brown glass bottles at -20ºC.

    Techniques: In Vitro, Cell Culture, Incubation

    In vivo Anti-Tumor Activity of Gimatecan in HCC Xenograft Models. Four types of HCC cell lines, Huh-1, Hep G2, HCCLM3, and PLCPRF5 were inoculated subcutaneously on the right side of the mouse back, respectively. In each tumor-bearing model mice were divided into four groups (n = 10 for each group) and orally administered with 0.8 mg/kg (×), 0.4 mg/kg (◆), and 0.1 mg/kg (●) gimatecan every four days for a total of four times, respectively. The control mice were administered with 10 µl 10%DMSO/g (●). Tumor volume was measured and expressed in mm 3

    Journal: Asian Pacific Journal of Cancer Prevention : APJCP

    Article Title: In Vitro and In Vivo Anticancer Activity of Gimatecan against Hepatocellular Carcinoma

    doi: 10.22034/APJCP.2016.17.11.4853

    Figure Lengend Snippet: In vivo Anti-Tumor Activity of Gimatecan in HCC Xenograft Models. Four types of HCC cell lines, Huh-1, Hep G2, HCCLM3, and PLCPRF5 were inoculated subcutaneously on the right side of the mouse back, respectively. In each tumor-bearing model mice were divided into four groups (n = 10 for each group) and orally administered with 0.8 mg/kg (×), 0.4 mg/kg (◆), and 0.1 mg/kg (●) gimatecan every four days for a total of four times, respectively. The control mice were administered with 10 µl 10%DMSO/g (●). Tumor volume was measured and expressed in mm 3

    Article Snippet: Stock solutions of gimatecan were dissolved in 100% DMSO (Amresco, USA) and stored in sterilized brown glass bottles at -20ºC.

    Techniques: In Vivo, Activity Assay, Mouse Assay

    Gimatecan Administration Did Not Severely Affect Body Weights. Four types of HCC cell lines, Huh-1, Hep G2, HCCLM3, and PLCPRF5 were inoculated subcutaneously on the right side of the mouse back, respectively. In each tumor-bearing model mice were divided into four groups (n = 10 for each group) and orally administered with 0.8 mg/kg (×), 0.4 mg/kg (◆), and 0.1 mg/kg (●) gimatecan every four days for a total of four times, respectively. The control mice were administered with 10 µl 10%DMSO/g (●). Mouse body weights were measured twice weekly and at study termination.

    Journal: Asian Pacific Journal of Cancer Prevention : APJCP

    Article Title: In Vitro and In Vivo Anticancer Activity of Gimatecan against Hepatocellular Carcinoma

    doi: 10.22034/APJCP.2016.17.11.4853

    Figure Lengend Snippet: Gimatecan Administration Did Not Severely Affect Body Weights. Four types of HCC cell lines, Huh-1, Hep G2, HCCLM3, and PLCPRF5 were inoculated subcutaneously on the right side of the mouse back, respectively. In each tumor-bearing model mice were divided into four groups (n = 10 for each group) and orally administered with 0.8 mg/kg (×), 0.4 mg/kg (◆), and 0.1 mg/kg (●) gimatecan every four days for a total of four times, respectively. The control mice were administered with 10 µl 10%DMSO/g (●). Mouse body weights were measured twice weekly and at study termination.

    Article Snippet: Stock solutions of gimatecan were dissolved in 100% DMSO (Amresco, USA) and stored in sterilized brown glass bottles at -20ºC.

    Techniques: Mouse Assay

    Effects of GYY4137 on the rat DLNCs. The DLNCs were isolated from the rats immunized with MOG + CFA. The percentage of CD4+ CD25+ FoxP3+ cells (Treg), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg was determined among the DLNCs ( A ) or among CD4+ T cells purified from the DLNCs ( B ), after 40 min of cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). The percentage of Th17 cells was determined among the DLNCs, treated with GYY4137 (GYY) or DMSO as the vehicle (DMSO) for 40 min and subsequently stimulated for 4 h ( C ). In some experiments, the cultures without DMSO (Ctrl) were also performed ( A , C ). IL-17 and IFN-γ cytokine concentrations in the supernatants of the 24 h cell cultures of MOG re-stimulated DLNCs and treated with GYY4137, were determined by ELISA ( D ). Data are presented as the mean + standard deviation (SD) from three ( C ), four ( B ) or six samples ( A , D ). * p

    Journal: Antioxidants

    Article Title: Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis

    doi: 10.3390/antiox9070608

    Figure Lengend Snippet: Effects of GYY4137 on the rat DLNCs. The DLNCs were isolated from the rats immunized with MOG + CFA. The percentage of CD4+ CD25+ FoxP3+ cells (Treg), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg was determined among the DLNCs ( A ) or among CD4+ T cells purified from the DLNCs ( B ), after 40 min of cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). The percentage of Th17 cells was determined among the DLNCs, treated with GYY4137 (GYY) or DMSO as the vehicle (DMSO) for 40 min and subsequently stimulated for 4 h ( C ). In some experiments, the cultures without DMSO (Ctrl) were also performed ( A , C ). IL-17 and IFN-γ cytokine concentrations in the supernatants of the 24 h cell cultures of MOG re-stimulated DLNCs and treated with GYY4137, were determined by ELISA ( D ). Data are presented as the mean + standard deviation (SD) from three ( C ), four ( B ) or six samples ( A , D ). * p

    Article Snippet: GYY4137 was initially diluted in DMSO (Sigma-Aldrich) and DMSO was used as the vehicle control in all the experiments.

    Techniques: Isolation, Purification, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Effects of GYY4137 on bone marrow-derived dendritic cells (BMDCs). BMDCs were propagated from mouse bone marrow precursors in the presence of Granulocyte-macrophage colony-stimulating factor (GM-CSF) and matured under the influence of lipopolysaccharide (LPS). Moreover, 200 μM GYY4137 (GYY) was applied simultaneously with LPS and DMSO was used as the vehicle control (DMSO). The cell viability was determined by the MTT test ( A ), the expression of MHC II, CD80 and CD40 was determined by cytofluorimetry ( B ), the mRNA expression relative to β-actin was detected by real-time RT-PCR ( C ), the cytokine concentrations were determined by ELISA ( D ), phagocytosis was determined by cytofluorimetry ( E ), and reactive oxygen species (ROS) production was measured by DHR staining and cytofluorimetry ( F ). Data are presented as the mean + standard deviation (SD) from three ( F ), four ( B ), five ( A , C , E ) or six ( D ) samples. * p

    Journal: Antioxidants

    Article Title: Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis

    doi: 10.3390/antiox9070608

    Figure Lengend Snippet: Effects of GYY4137 on bone marrow-derived dendritic cells (BMDCs). BMDCs were propagated from mouse bone marrow precursors in the presence of Granulocyte-macrophage colony-stimulating factor (GM-CSF) and matured under the influence of lipopolysaccharide (LPS). Moreover, 200 μM GYY4137 (GYY) was applied simultaneously with LPS and DMSO was used as the vehicle control (DMSO). The cell viability was determined by the MTT test ( A ), the expression of MHC II, CD80 and CD40 was determined by cytofluorimetry ( B ), the mRNA expression relative to β-actin was detected by real-time RT-PCR ( C ), the cytokine concentrations were determined by ELISA ( D ), phagocytosis was determined by cytofluorimetry ( E ), and reactive oxygen species (ROS) production was measured by DHR staining and cytofluorimetry ( F ). Data are presented as the mean + standard deviation (SD) from three ( F ), four ( B ), five ( A , C , E ) or six ( D ) samples. * p

    Article Snippet: GYY4137 was initially diluted in DMSO (Sigma-Aldrich) and DMSO was used as the vehicle control in all the experiments.

    Techniques: Derivative Assay, MTT Assay, Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Staining, Standard Deviation

    Effects of GYY4137 on the mouse draining lymph node cells (DLNCs). The DLNCs were isolated from the mice immunized with myeline oligodendrocyte glycoprotein (MOG) + complete Freund’s adjuvant (CFA). The percentage of CD4+ CD25+ FoxP3+ cells (regulatory T cells (Treg)), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg among DLNCs was measured after different time points of treatment with 200 μM GYY4137 (GYY) or DMSO as the solvent control (DMSO) ( A ). The percentage of Treg among the DLNCs was measured after 40 min of treatment with 200 μM of spent GYY4137 (GYYspent) or spent DMSO as the solvent control (DMSOspent) ( B ), or with Na2S 200 μM or no treatment (Ctrl) ( C ). Pe rcentage of IL-17+ cells among CD4+ cells was determined among the DLNCs, treated with GYY4137 (GYY) or DMSO as the vehicle (DMSO) for 40 min and subsequently stimulated for 4 h or 16 h ( D ). IL-17 and IFN-γ cytokine concentrations in the supernatants of 24 h cell cultures of MOG re-stimulated DLNCs treated with GYY4137 were determined by ELISA ( E ). The data are presented as the mean + standard deviation (SD) from three ( A – C ) or six ( D , E ) samples. * p

    Journal: Antioxidants

    Article Title: Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis

    doi: 10.3390/antiox9070608

    Figure Lengend Snippet: Effects of GYY4137 on the mouse draining lymph node cells (DLNCs). The DLNCs were isolated from the mice immunized with myeline oligodendrocyte glycoprotein (MOG) + complete Freund’s adjuvant (CFA). The percentage of CD4+ CD25+ FoxP3+ cells (regulatory T cells (Treg)), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg among DLNCs was measured after different time points of treatment with 200 μM GYY4137 (GYY) or DMSO as the solvent control (DMSO) ( A ). The percentage of Treg among the DLNCs was measured after 40 min of treatment with 200 μM of spent GYY4137 (GYYspent) or spent DMSO as the solvent control (DMSOspent) ( B ), or with Na2S 200 μM or no treatment (Ctrl) ( C ). Pe rcentage of IL-17+ cells among CD4+ cells was determined among the DLNCs, treated with GYY4137 (GYY) or DMSO as the vehicle (DMSO) for 40 min and subsequently stimulated for 4 h or 16 h ( D ). IL-17 and IFN-γ cytokine concentrations in the supernatants of 24 h cell cultures of MOG re-stimulated DLNCs treated with GYY4137 were determined by ELISA ( E ). The data are presented as the mean + standard deviation (SD) from three ( A – C ) or six ( D , E ) samples. * p

    Article Snippet: GYY4137 was initially diluted in DMSO (Sigma-Aldrich) and DMSO was used as the vehicle control in all the experiments.

    Techniques: Isolation, Mouse Assay, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Effects of GYY4137 on rat spinal cord immune cells (SCICs). SCICs and DLNCs were isolated from rats immunized with rat spinal cord homogenate (SCH) + CFA at the peak of the disease or at day 7 post immunization, respectively. Clinical course of the EAE is presented ( A ). The percentage of the CD4+ CD25+ FoxP3+ cells (Treg), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg was determined among the SCICs after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO) ( B ) The percentage of IL-17+ cells among the CD4+ cells was determined among the SCICs ( C ) or among the CD4+ T cells purified from the SCICs ( D ), after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). The percentage of Treg was determined among the DLNCs after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO) ( E ). The percentage of IL-17+ cells among the CD4+ cells was determined among the DLNCs ( F ) after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). In some experiments, the cultures without DMSO (Ctrl) were also performed ( B , C ). IL-17 and IFN-γ cytokine concentrations in the supernatants of 24 h cell cultures of SCICs treated with GYY4137 were determined by ELISA ( G ). Data are presented as the mean + standard deviation (SD) from three ( C , D , F ), four ( B , E ) or six ( A , G ) samples. * p

    Journal: Antioxidants

    Article Title: Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis

    doi: 10.3390/antiox9070608

    Figure Lengend Snippet: Effects of GYY4137 on rat spinal cord immune cells (SCICs). SCICs and DLNCs were isolated from rats immunized with rat spinal cord homogenate (SCH) + CFA at the peak of the disease or at day 7 post immunization, respectively. Clinical course of the EAE is presented ( A ). The percentage of the CD4+ CD25+ FoxP3+ cells (Treg), and the proportion of IL17+ among the CD4+ cells were determined by cytofluorimetry. The percentage of Treg was determined among the SCICs after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO) ( B ) The percentage of IL-17+ cells among the CD4+ cells was determined among the SCICs ( C ) or among the CD4+ T cells purified from the SCICs ( D ), after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). The percentage of Treg was determined among the DLNCs after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO) ( E ). The percentage of IL-17+ cells among the CD4+ cells was determined among the DLNCs ( F ) after 40 min cultivation in the presence of 200 μM GYY4137 (GYY) or DMSO as the vehicle (DMSO). In some experiments, the cultures without DMSO (Ctrl) were also performed ( B , C ). IL-17 and IFN-γ cytokine concentrations in the supernatants of 24 h cell cultures of SCICs treated with GYY4137 were determined by ELISA ( G ). Data are presented as the mean + standard deviation (SD) from three ( C , D , F ), four ( B , E ) or six ( A , G ) samples. * p

    Article Snippet: GYY4137 was initially diluted in DMSO (Sigma-Aldrich) and DMSO was used as the vehicle control in all the experiments.

    Techniques: Isolation, Purification, Enzyme-linked Immunosorbent Assay, Standard Deviation