ro15 Search Results


90
TargetMol flumazenil
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Flumazenil, supplied by TargetMol, 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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MedChemExpress flumazenil
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Flumazenil, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Revvity 3h ro15 1788
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
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ro15  (Tocris)
91
Tocris ro15
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
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Revvity h ro15 4513
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
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92
MedChemExpress hy b1894a cefditoren cdn third approved
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Hy B1894a Cefditoren Cdn Third Approved, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress musechem
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Musechem, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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NEN Life Science methyl-3h]ro15-1788
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Methyl 3h]Ro15 1788, supplied by NEN Life Science, 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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Balster Einheitserdewerk ro 15-4513
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
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New England Nuclear Corporation zv-methyl-3h]ro 15-1788
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
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Biotrend Chemicals flumazenil (ro15-1788; ethyl 8-fluoro-5-methyl-6-oxo-5,6-dihydro-4 h -benzo[ f ]imidazo[1,5- a ][1,4]diazepine-3-carboxylate)
Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of <t>flumazenil</t> (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .
Flumazenil (Ro15 1788; Ethyl 8 Fluoro 5 Methyl 6 Oxo 5,6 Dihydro 4 H Benzo[ F ]Imidazo[1,5 A ][1,4]Diazepine 3 Carboxylate), supplied by Biotrend Chemicals, 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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Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of flumazenil (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .

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

Article Title: Neutralization of acyl-CoA-binding protein attenuates glucocorticoid-mediated suppression of cancer immunosurveillance

doi: 10.1073/pnas.2518983123

Figure Lengend Snippet: Modulation of antigen cross-presentation and Tsc22d3/TSC22D3 expression by ACBP/DBI neutralization in dendritic cells under glucocorticoid treatment. ( A ) The heatmap depicts the gene expression levels of mouse GM-CSF BMDCs isolated after 18 h of different treatments as indicated: vehicle; corticosterone (CORT, 1 μM); αDBI antibody (2.5 μg/mL) or its isotype (2.5 μg/mL). The computed P -values are presented in squares with different colors. Statistical analyses were performed by one-way ANOVA with Tukey correction. Tsc22d3 mRNA levels were measured by RT-qPCR in mouse BMDCs treated with corticosterone (CORT, 1 µM) in the presence or absence of flumazenil (1 µM) or bicuculline (10 µM) ( B ), or in Gabrg2 wild-type ( Gabrg2 WT/WT ) or Gabrg2 knock-in ( Gabrg2 F77I/F77I ) backgrounds ( C ). Tsc22d3/TSC22D3 expression was further assessed in mouse splenocytes ( D ) exposed to corticosterone (CORT, 1 µM), in human peripheral blood mononuclear cells (PBMCs; E ) and human monocyte-derived dendritic cells (moDCs; F ) exposed to hydrocortisone (HCS, 0.5 µM), each treated in the presence or absence of an ACBP/DBI-neutralizing antibody (αDBI; 2,5 µg/mL), as indicated. For panels ( B – F ), gene expression was quantified by RT-qPCR, normalized to housekeeping gene expression, and expressed as fold change relative to the corresponding untreated control condition within each experiment. Data are presented as columns with individual data points overlaid and shown as mean ± SEM. Statistical analyses were performed using ANOVA with correction for multiple comparisons; exact P values are indicated above the corresponding comparisons. ( G – I ) Upon CORT treatment, the efficacy of oxaliplatin (OXA; 5 mg/kg; i.p.) combined with either αPD1 antibody or its isotype control (200 µg/mouse; i.p.) and αDBI antibody or its isotype control (5 mg/kg) was assessed against MCA205 tumors in LysM-creX Tsc22d3 +/+ (n = 4 to 13 mice per group) ( H ) or LysM-creX Tsc22d3 −/− (n = 5 to 12 mice per group) ( I ) 8 to 10-wk-old male mice. Statistical analysis was performed using mixed linear model of tumor growth ( https://kroemerlab.shinyapps.io/TumGrowth/ ). Computed P -values are reported in panels H and I .

Article Snippet: Flumazenil (TopScience, #78755-81-4), bicuculline (MedChemExpress, #HY-N0219), corticosterone (Sigma-Aldrich, #27840), and hydrocortisone (MedChemExpress, Cat# HY-N0583) were dissolved in DMSO to prepare stock solutions and diluted in culture medium to the indicated working concentrations immediately before use.

Techniques: Expressing, Neutralization, Gene Expression, Isolation, Quantitative RT-PCR, Knock-In, Derivative Assay, Control