short interfering rna sirna Search Results


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  • 99
    Millipore mission shrna lentiviral particles against epcam
    MM-131 inhibits cancer cell proliferation and migration. MM-131 blocks HGF-dependent cell proliferation ( A ) and proliferation of MET -amplified cells ( B ) in a dose-dependent manner. NCI-H747, NCI-H441, and MKN-45 cell lines were stably transduced with <t>lentiviral</t> particles expressing untargeted <t>shRNA</t> (shControl) or shRNA targeting <t>EpCAM</t> (shEpCAM). Following formation of 3D spheroids, cells were treated with the indicated antibodies for 96 h. Viability was assessed by CellTiter-Glo assay and normalized to vehicle-treated cells in the presence ( A ) or absence ( B ) of 1 nM HGF. ( C ) MM-131 blocks HGF-induced cell migration in a dose-dependent manner. Following production of a uniform scratch wound, images were taken every 2 h for 24 h. Migration rates were calculated from the relative wound densities (density of cells inside the wound area/density outside the wound area) of each image and normalized to vehicle-treated cells in the presence of 1 nM HGF. ( D ) Unlike huOA-5D5 and LY2875358, MM-131 does not promote migration in the absence of HGF. A scratch wound migration assay was performed as in C , except in the absence of HGF. Migration rates were normalized to vehicle-treated cells in the absence of HGF. ( E ) Representative images of NCI-H441 cells from an HGF-induced migration assay. Images are from 1 μM treatment of indicated molecules. The wound area remaining is shown in gray, and the confluence mask is shown in orange. All plots reflect mean ( n = 3) and SEM.
    Mission Shrna Lentiviral Particles Against Epcam, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Sirna Therapeutics short interfering rna sirna
    MM-131 inhibits cancer cell proliferation and migration. MM-131 blocks HGF-dependent cell proliferation ( A ) and proliferation of MET -amplified cells ( B ) in a dose-dependent manner. NCI-H747, NCI-H441, and MKN-45 cell lines were stably transduced with <t>lentiviral</t> particles expressing untargeted <t>shRNA</t> (shControl) or shRNA targeting <t>EpCAM</t> (shEpCAM). Following formation of 3D spheroids, cells were treated with the indicated antibodies for 96 h. Viability was assessed by CellTiter-Glo assay and normalized to vehicle-treated cells in the presence ( A ) or absence ( B ) of 1 nM HGF. ( C ) MM-131 blocks HGF-induced cell migration in a dose-dependent manner. Following production of a uniform scratch wound, images were taken every 2 h for 24 h. Migration rates were calculated from the relative wound densities (density of cells inside the wound area/density outside the wound area) of each image and normalized to vehicle-treated cells in the presence of 1 nM HGF. ( D ) Unlike huOA-5D5 and LY2875358, MM-131 does not promote migration in the absence of HGF. A scratch wound migration assay was performed as in C , except in the absence of HGF. Migration rates were normalized to vehicle-treated cells in the absence of HGF. ( E ) Representative images of NCI-H441 cells from an HGF-induced migration assay. Images are from 1 μM treatment of indicated molecules. The wound area remaining is shown in gray, and the confluence mask is shown in orange. All plots reflect mean ( n = 3) and SEM.
    Short Interfering Rna Sirna, supplied by Sirna Therapeutics, used in various techniques. Bioz Stars score: 91/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Thermo Fisher short interfering rna sirna sirnas
    Effects of galectin-1 on the Ras-transmitted downstream signals. Scrambled <t>RNA</t> or galectin-1 <t>shRNA</t> were transfected in HeLa cells. GFP or galectin-1 cDNA were transfected in C33A cells. The cells were irradiated with 6 Gy and harvested 5 or 10 min later. Expressions of activated H-Ras, p-Raf-1, and p-ERK using western blots in HeLa and C33A cells were compared with or without galectin-1 modulation
    Short Interfering Rna Sirna Sirnas, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Thermo Fisher short hairpin rna shrna
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Hairpin Rna Shrna, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 822 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology short interfering rna sirna sirnas
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Interfering Rna Sirna Sirnas, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ribobio short interfering rna sirna fragments
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Interfering Rna Sirna Fragments, supplied by Ribobio, used in various techniques. Bioz Stars score: 88/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology control short interfering rna sirna
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Control Short Interfering Rna Sirna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher short interfering rna transfection stealth short interfering rna sirna
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Interfering Rna Transfection Stealth Short Interfering Rna Sirna, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 89/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GE Healthcare short interfering rna sirna pools
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Interfering Rna Sirna Pools, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 90/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Kaneka Corp short interfering rna sirna dimers
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Short Interfering Rna Sirna Dimers, supplied by Kaneka Corp, used in various techniques. Bioz Stars score: 85/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GE Healthcare sirna transfection short interfering rnas sirna
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Sirna Transfection Short Interfering Rnas Sirna, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Kaneka Corp sirna transfection short interfering rnas sirnas
    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control <t>shRNA</t> or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total <t>RNA</t> in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P
    Sirna Transfection Short Interfering Rnas Sirnas, supplied by Kaneka Corp, used in various techniques. Bioz Stars score: 88/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology gab2 short interfering rna sirna
    Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and <t>Gab2</t> <t>siRNA,</t> before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P
    Gab2 Short Interfering Rna Sirna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Horizon Discovery control short interfering rna sirna pool
    Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and <t>Gab2</t> <t>siRNA,</t> before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P
    Control Short Interfering Rna Sirna Pool, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 85/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Horizon Discovery short interfering rna sirna otp smartpools
    Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and <t>Gab2</t> <t>siRNA,</t> before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P
    Short Interfering Rna Sirna Otp Smartpools, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Horizon Discovery p2y4 short interfering rna sirna
    Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and <t>Gab2</t> <t>siRNA,</t> before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P
    P2y4 Short Interfering Rna Sirna, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Horizon Discovery small interfering rna sirna oligos
    Knockdown of Atg5 protein by <t>siRNA</t> <t>oligos.</t> Human blood macrophages were transfected with siAtg5 or siCtrl at 100 and 200 nM. At 48 hour post-transfection, whole-cell lysates were harvested and Atg5 expression was measured by western blot
    Small Interfering Rna Sirna Oligos, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 88/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher short interfering rna sirna smartpool rna duplexes
    Knockdown of Atg5 protein by <t>siRNA</t> <t>oligos.</t> Human blood macrophages were transfected with siAtg5 or siCtrl at 100 and 200 nM. At 48 hour post-transfection, whole-cell lysates were harvested and Atg5 expression was measured by western blot
    Short Interfering Rna Sirna Smartpool Rna Duplexes, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Horizon Discovery smartpool small interfering rna sirna
    Effects of <t>siRNA-AdipoR1</t> transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total <t>RNA</t> was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.
    Smartpool Small Interfering Rna Sirna, supplied by Horizon Discovery, used in various techniques. Bioz Stars score: 88/100, based on 124 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Qiagen short interfering rna sirna duplexes
    Effects of <t>siRNA-AdipoR1</t> transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total <t>RNA</t> was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.
    Short Interfering Rna Sirna Duplexes, supplied by Qiagen, used in various techniques. Bioz Stars score: 99/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effects of <t>siRNA-AdipoR1</t> transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total <t>RNA</t> was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.
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    Effects of <t>siRNA-AdipoR1</t> transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total <t>RNA</t> was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.
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    Effects of <t>siRNA-AdipoR1</t> transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total <t>RNA</t> was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.
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    Image Search Results


    MM-131 inhibits cancer cell proliferation and migration. MM-131 blocks HGF-dependent cell proliferation ( A ) and proliferation of MET -amplified cells ( B ) in a dose-dependent manner. NCI-H747, NCI-H441, and MKN-45 cell lines were stably transduced with lentiviral particles expressing untargeted shRNA (shControl) or shRNA targeting EpCAM (shEpCAM). Following formation of 3D spheroids, cells were treated with the indicated antibodies for 96 h. Viability was assessed by CellTiter-Glo assay and normalized to vehicle-treated cells in the presence ( A ) or absence ( B ) of 1 nM HGF. ( C ) MM-131 blocks HGF-induced cell migration in a dose-dependent manner. Following production of a uniform scratch wound, images were taken every 2 h for 24 h. Migration rates were calculated from the relative wound densities (density of cells inside the wound area/density outside the wound area) of each image and normalized to vehicle-treated cells in the presence of 1 nM HGF. ( D ) Unlike huOA-5D5 and LY2875358, MM-131 does not promote migration in the absence of HGF. A scratch wound migration assay was performed as in C , except in the absence of HGF. Migration rates were normalized to vehicle-treated cells in the absence of HGF. ( E ) Representative images of NCI-H441 cells from an HGF-induced migration assay. Images are from 1 μM treatment of indicated molecules. The wound area remaining is shown in gray, and the confluence mask is shown in orange. All plots reflect mean ( n = 3) and SEM.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: MM-131, a bispecific anti-Met/EpCAM mAb, inhibits HGF-dependent and HGF-independent Met signaling through concurrent binding to EpCAM

    doi: 10.1073/pnas.1819085116

    Figure Lengend Snippet: MM-131 inhibits cancer cell proliferation and migration. MM-131 blocks HGF-dependent cell proliferation ( A ) and proliferation of MET -amplified cells ( B ) in a dose-dependent manner. NCI-H747, NCI-H441, and MKN-45 cell lines were stably transduced with lentiviral particles expressing untargeted shRNA (shControl) or shRNA targeting EpCAM (shEpCAM). Following formation of 3D spheroids, cells were treated with the indicated antibodies for 96 h. Viability was assessed by CellTiter-Glo assay and normalized to vehicle-treated cells in the presence ( A ) or absence ( B ) of 1 nM HGF. ( C ) MM-131 blocks HGF-induced cell migration in a dose-dependent manner. Following production of a uniform scratch wound, images were taken every 2 h for 24 h. Migration rates were calculated from the relative wound densities (density of cells inside the wound area/density outside the wound area) of each image and normalized to vehicle-treated cells in the presence of 1 nM HGF. ( D ) Unlike huOA-5D5 and LY2875358, MM-131 does not promote migration in the absence of HGF. A scratch wound migration assay was performed as in C , except in the absence of HGF. Migration rates were normalized to vehicle-treated cells in the absence of HGF. ( E ) Representative images of NCI-H441 cells from an HGF-induced migration assay. Images are from 1 μM treatment of indicated molecules. The wound area remaining is shown in gray, and the confluence mask is shown in orange. All plots reflect mean ( n = 3) and SEM.

    Article Snippet: To generate EpCAM knockdown cell lines, cells were transduced with Mission shRNA lentiviral particles against EpCAM (SHCLNV- ; Sigma–Aldrich).

    Techniques: Migration, Amplification, Stable Transfection, Transduction, Expressing, shRNA, Glo Assay

    Effects of galectin-1 on the Ras-transmitted downstream signals. Scrambled RNA or galectin-1 shRNA were transfected in HeLa cells. GFP or galectin-1 cDNA were transfected in C33A cells. The cells were irradiated with 6 Gy and harvested 5 or 10 min later. Expressions of activated H-Ras, p-Raf-1, and p-ERK using western blots in HeLa and C33A cells were compared with or without galectin-1 modulation

    Journal: Cell Death & Disease

    Article Title: A novel radioresistant mechanism of galectin-1 mediated by H-Ras-dependent pathways in cervical cancer cells

    doi: 10.1038/cddis.2011.120

    Figure Lengend Snippet: Effects of galectin-1 on the Ras-transmitted downstream signals. Scrambled RNA or galectin-1 shRNA were transfected in HeLa cells. GFP or galectin-1 cDNA were transfected in C33A cells. The cells were irradiated with 6 Gy and harvested 5 or 10 min later. Expressions of activated H-Ras, p-Raf-1, and p-ERK using western blots in HeLa and C33A cells were compared with or without galectin-1 modulation

    Article Snippet: Short interfering RNA (siRNA) siRNAs (Invitrogen) were used to silence galectin-1, H-Ras, or K-Ras according to the protocol provided by the manufacturer. siRNA (7.5 μ l) and Opti-MEM (250 μ l) were mixed.

    Techniques: shRNA, Transfection, Irradiation, Western Blot

    Galectin-1-mediated radioresistance was dependent on H-Ras but not on K-Ras. The knock down of HeLa cells by the siRNA of galectin-1 and H-Ras was confirmed by reverse transcription-polymerase chain reaction analysis and western-blot analysis in cells transfected with siRNA. Control cells were treated with scrambled RNA. The clonogenic survival curves were compared among scrambled RNA, H-Ras knockdown/scrambled RNA, and H-Ras knockdown/galectin-1 knockdown. After 48 h following transfection, cells were irradiated, and a clonogenic assay was performed 12 to 14 days after irradiation. Galectin-1 ( a ) knockdown or ( b ) overexpression did not affect the radiosensitivity of cervical cancer cells with H-Ras knockdown. However, galectin-1 ( c ) knockdown or ( d ) overexpression altered the radiosensitivity of cervical cancer cells with K-Ras knockdown. ( e ) Galectin-1 knockdown decreased clonogenic survival in HeLa cells transfected with mutated H-Ras at high doses but not at low doses. Clonogenic assays were performed during three independent experiments at each paired condition (with and without galectin-1 modulation). The error bar represents the standard error of mean: * P

    Journal: Cell Death & Disease

    Article Title: A novel radioresistant mechanism of galectin-1 mediated by H-Ras-dependent pathways in cervical cancer cells

    doi: 10.1038/cddis.2011.120

    Figure Lengend Snippet: Galectin-1-mediated radioresistance was dependent on H-Ras but not on K-Ras. The knock down of HeLa cells by the siRNA of galectin-1 and H-Ras was confirmed by reverse transcription-polymerase chain reaction analysis and western-blot analysis in cells transfected with siRNA. Control cells were treated with scrambled RNA. The clonogenic survival curves were compared among scrambled RNA, H-Ras knockdown/scrambled RNA, and H-Ras knockdown/galectin-1 knockdown. After 48 h following transfection, cells were irradiated, and a clonogenic assay was performed 12 to 14 days after irradiation. Galectin-1 ( a ) knockdown or ( b ) overexpression did not affect the radiosensitivity of cervical cancer cells with H-Ras knockdown. However, galectin-1 ( c ) knockdown or ( d ) overexpression altered the radiosensitivity of cervical cancer cells with K-Ras knockdown. ( e ) Galectin-1 knockdown decreased clonogenic survival in HeLa cells transfected with mutated H-Ras at high doses but not at low doses. Clonogenic assays were performed during three independent experiments at each paired condition (with and without galectin-1 modulation). The error bar represents the standard error of mean: * P

    Article Snippet: Short interfering RNA (siRNA) siRNAs (Invitrogen) were used to silence galectin-1, H-Ras, or K-Ras according to the protocol provided by the manufacturer. siRNA (7.5 μ l) and Opti-MEM (250 μ l) were mixed.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Irradiation, Clonogenic Assay, Over Expression

    Galectin-1 enhanced the repair of DNA damage. GFP or galectin-1 plus GFP were transfected into C33A cells. Stable clones of scrambled RNA or galectin-1 shRNA were transfected into HeLa cells. Cells were harvested immediately, 4 or 24 h following 6-Gy irradiation. Comet assay was performed. ( a ) A longer tail was noted in galectin-1 shRNA compared with scrambled RNA HeLa cells 24 h following irradiation. ( b ) A shorter tail was noted in galectin-1-overexpressed cells compared with GFP-transfected C33A cells 24 h following irradiation. ( c ) Western blots were performed after harvesting the cells. Greater γ -H2AX expression was noted in galectin-1-knocked down HeLa cells and GFP-transfected C33A cells 4 h and 24 h following irradiation, respectively

    Journal: Cell Death & Disease

    Article Title: A novel radioresistant mechanism of galectin-1 mediated by H-Ras-dependent pathways in cervical cancer cells

    doi: 10.1038/cddis.2011.120

    Figure Lengend Snippet: Galectin-1 enhanced the repair of DNA damage. GFP or galectin-1 plus GFP were transfected into C33A cells. Stable clones of scrambled RNA or galectin-1 shRNA were transfected into HeLa cells. Cells were harvested immediately, 4 or 24 h following 6-Gy irradiation. Comet assay was performed. ( a ) A longer tail was noted in galectin-1 shRNA compared with scrambled RNA HeLa cells 24 h following irradiation. ( b ) A shorter tail was noted in galectin-1-overexpressed cells compared with GFP-transfected C33A cells 24 h following irradiation. ( c ) Western blots were performed after harvesting the cells. Greater γ -H2AX expression was noted in galectin-1-knocked down HeLa cells and GFP-transfected C33A cells 4 h and 24 h following irradiation, respectively

    Article Snippet: Short interfering RNA (siRNA) siRNAs (Invitrogen) were used to silence galectin-1, H-Ras, or K-Ras according to the protocol provided by the manufacturer. siRNA (7.5 μ l) and Opti-MEM (250 μ l) were mixed.

    Techniques: Transfection, Clone Assay, shRNA, Irradiation, Single Cell Gel Electrophoresis, Western Blot, Expressing

    JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control shRNA or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total RNA in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P

    Journal: Nucleic Acids Research

    Article Title: JWA regulates XRCC1 and functions as a novel base excision repair protein in oxidative-stress-induced DNA single-strand breaks

    doi: 10.1093/nar/gkp054

    Figure Lengend Snippet: JWA regulates XRCC1 transcription via the MAPK signaling pathway and E2F1. ( A ) JWA knockdown in NIH-3T3 cells significantly inhibits H 2 O 2 -induced transcription of XRCC1. NIH-3T3 cells were transfected with a control shRNA or a JWA shRNA plasmid, followed by treatment with or without 100 μM H 2 O 2 for 30 min. Levels of JWA and XRCC1 transcription were detected by quantitative RT-PCR, and GAPDH was used as an endogenous control to normalize the differences in the amount of total RNA in each sample. ( B ) The E2F1-binding domain in the XRCC1 promoter is required for the JWA-mediated increase in XRCC1 expression after exposure to H 2 O 2 . NIH-3T3 cells were co-transfected with either control shRNA or JWA shRNA, together with the XRCC1 promoter-reporter (–881 to + 158, containing E2F1-binding domain) or an E2F1-binding site deleted XRCC1 promoter-reporter (ΔE2F1-XRCC1, –776 to + 158). After 24 h, the transfected cells were cultured with or without 100 μM H 2 O 2 for 30 min, then the reporter activity was examined. The means ± SD of triplicate experiments are shown. * P

    Article Snippet: The JWA siRNA Expression Cassette and scrambled short-hairpin RNA (shRNA) ( ) were subcloned into the linearized vector pSEC (Ambion, Austin, TX, USA) to produce JWA shRNA and control shRNA plasmids, respectively.

    Techniques: Transfection, shRNA, Plasmid Preparation, Quantitative RT-PCR, Binding Assay, Expressing, Cell Culture, Activity Assay

    Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and Gab2 siRNA, before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P

    Journal: PLoS ONE

    Article Title: The Inhibition of Mast Cell Activation of Radix Paeoniae alba Extraction Identified by TCRP Based and Conventional Cell Function Assay Systems

    doi: 10.1371/journal.pone.0155930

    Figure Lengend Snippet: Construction of IgE-mediated mast cell TCRPs. (A) IgE-mediated TCRPs for functional monitoring of mast cell degranulation. RBL-2H3 mast cells were cultured on E-plates at a density of 10,000 cells/well, and incubated with 100 ng/mL anti-DNP IgE approximately 22 h later. After sensitization overnight, the cells were stimulated with 100 ng/mL DNP-BSA. The impedance expressed as the cell index (CI), was continuously monitored. (B) Pharmacological inhibitors of FcεRI receptor-activated downstream signal pathways that significantly attenuated IgE-mediated TCRPs. IgE sensitized RBL-2H3 cells were seed on the E-plates overnight at a density of 20,000 cells/well, and pre-treated with the inhibitors PP1, PD98059, bisindoylmaleimide I and Gab2 siRNA, before stimulation with DNP-BSA. (C) Mediator release assay of RBL-2H3 mast cell activation. RBL-2H3 cells were sensitized with 100 ng/mL IgE and activated by the addition of 100 ng/mL DNP-BSA. β-hexosaminidase activities were measured at the indicated time. **, P

    Article Snippet: Gab2 short interfering RNA (siRNA) was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Functional Assay, Cell Culture, Incubation, Release Assay, Activation Assay

    Knockdown of Atg5 protein by siRNA oligos. Human blood macrophages were transfected with siAtg5 or siCtrl at 100 and 200 nM. At 48 hour post-transfection, whole-cell lysates were harvested and Atg5 expression was measured by western blot

    Journal: Cellular and Molecular Immunology

    Article Title: Cellular response to influenza virus infection: a potential role for autophagy in CXCL10 and interferon-alpha induction

    doi: 10.1038/cmi.2010.25

    Figure Lengend Snippet: Knockdown of Atg5 protein by siRNA oligos. Human blood macrophages were transfected with siAtg5 or siCtrl at 100 and 200 nM. At 48 hour post-transfection, whole-cell lysates were harvested and Atg5 expression was measured by western blot

    Article Snippet: Small interfering RNA (siRNA) oligos specific to Atg5 (siAtg5) and non-targeting siRNA oligos (siCtrl) were purchased from Dharmacon (Lafayette, CO, USA).

    Techniques: Transfection, Expressing, Western Blot

    Effects of siRNA-AdipoR1 transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.

    Journal: BMC Cell Biology

    Article Title: Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells

    doi: 10.1186/1471-2121-8-51

    Figure Lengend Snippet: Effects of siRNA-AdipoR1 transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Real-time PCR was performed as described in MATERIALS AND METHODS. Osterix mRNA expressions was suppressed by blocking the receptor expression (A). AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days. Osterix mRNA expressions was enhanced by AICAR (B). The result was the representative of five different experiments.

    Article Snippet: SMARTpool small interfering RNA (siRNA) and SMARTpool reagents for AdipoR1, CypB and nonspecific control siRNA duplexes were designed and synthesized by Customer SMARTpool siRNA Design from Dharmacon (Lafayette, CO).

    Techniques: Transfection, Expressing, Real-time Polymerase Chain Reaction, Blocking Assay

    Effects of siRNA-AdipoR1 transfection or an AICAR treatment on Runx-2 mRNA and protein expressions in MC3T3-E1 cells. (A and B) Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection, and cell lysate was collected at 7 days after transfection. Real-time PCR and immunoprecipitation were performed as described in MATERIALS AND METHODS. Neither Runx-2 mRNA (A) nor its protein (B) expressions were changed by blocking the receptor expression. (C and D) AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days, and cell lysate was collected at 14 days. Neither Runx-2 mRNA (C) nor its protein (D) expressions were changed by AICAR. The result was the representative of five different experiments.

    Journal: BMC Cell Biology

    Article Title: Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells

    doi: 10.1186/1471-2121-8-51

    Figure Lengend Snippet: Effects of siRNA-AdipoR1 transfection or an AICAR treatment on Runx-2 mRNA and protein expressions in MC3T3-E1 cells. (A and B) Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection, and cell lysate was collected at 7 days after transfection. Real-time PCR and immunoprecipitation were performed as described in MATERIALS AND METHODS. Neither Runx-2 mRNA (A) nor its protein (B) expressions were changed by blocking the receptor expression. (C and D) AICAR (0.5 mM), an AMP kinase stimulator, was added after the cells reached confluency. Total RNA was collected at 14, 21, 28 days, and cell lysate was collected at 14 days. Neither Runx-2 mRNA (C) nor its protein (D) expressions were changed by AICAR. The result was the representative of five different experiments.

    Article Snippet: SMARTpool small interfering RNA (siRNA) and SMARTpool reagents for AdipoR1, CypB and nonspecific control siRNA duplexes were designed and synthesized by Customer SMARTpool siRNA Design from Dharmacon (Lafayette, CO).

    Techniques: Transfection, Real-time Polymerase Chain Reaction, Immunoprecipitation, Blocking Assay, Expressing

    Effects of siRNA-AdipoR1 transfection on the differentiation of MC3T3-E1 cells. Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Col-I (A) and OCN (B) mRNA expression were decreased by blocking the receptor expression. Results are expressed as fold increase over the control values at 4 days. The result was the representative of five different experiments. (C) ALP activity of siRNA-AdipoR1-transfected MC3T3-E1 cells. ALP activity was evaluated biochemically. ALP activity was significantly decreased compared to the control (*** p

    Journal: BMC Cell Biology

    Article Title: Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells

    doi: 10.1186/1471-2121-8-51

    Figure Lengend Snippet: Effects of siRNA-AdipoR1 transfection on the differentiation of MC3T3-E1 cells. Total RNA was collected at 4, 7, 10 days after siRNA-AdipoR1 transfection. Col-I (A) and OCN (B) mRNA expression were decreased by blocking the receptor expression. Results are expressed as fold increase over the control values at 4 days. The result was the representative of five different experiments. (C) ALP activity of siRNA-AdipoR1-transfected MC3T3-E1 cells. ALP activity was evaluated biochemically. ALP activity was significantly decreased compared to the control (*** p

    Article Snippet: SMARTpool small interfering RNA (siRNA) and SMARTpool reagents for AdipoR1, CypB and nonspecific control siRNA duplexes were designed and synthesized by Customer SMARTpool siRNA Design from Dharmacon (Lafayette, CO).

    Techniques: Transfection, Expressing, Blocking Assay, ALP Assay, Activity Assay

    Adiponectin R1 and R2 expression in MC3T3-E1 cells and effects of siRNA-AdipoR1 transfection. (A) Adiponectin receptor expression in MC3T3-E1 cells. Total RNA from the cells was subjected to RT-PCR. HPRT, house keeping gene, and AdipoR1 were visualized in a 2% agarose gel stained with ethidium bromide. AdipoR1 mRNA but not AdipoR2 was expressed in MC3T3-E1 cells, while both of them were expressed in 3T3-L1 cells, which were examined as a positive control. (B) Confirmation of the effect of siRNA-AdipoR1. The siRNA restrained only siAdipoR1, showing that its knock down effect was specific (p

    Journal: BMC Cell Biology

    Article Title: Adiponectin and AMP kinase activator stimulate proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells

    doi: 10.1186/1471-2121-8-51

    Figure Lengend Snippet: Adiponectin R1 and R2 expression in MC3T3-E1 cells and effects of siRNA-AdipoR1 transfection. (A) Adiponectin receptor expression in MC3T3-E1 cells. Total RNA from the cells was subjected to RT-PCR. HPRT, house keeping gene, and AdipoR1 were visualized in a 2% agarose gel stained with ethidium bromide. AdipoR1 mRNA but not AdipoR2 was expressed in MC3T3-E1 cells, while both of them were expressed in 3T3-L1 cells, which were examined as a positive control. (B) Confirmation of the effect of siRNA-AdipoR1. The siRNA restrained only siAdipoR1, showing that its knock down effect was specific (p

    Article Snippet: SMARTpool small interfering RNA (siRNA) and SMARTpool reagents for AdipoR1, CypB and nonspecific control siRNA duplexes were designed and synthesized by Customer SMARTpool siRNA Design from Dharmacon (Lafayette, CO).

    Techniques: Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Staining, Positive Control