cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.31153408.v1
title: Figure 4F-G primary data

description: Fig 4. TBK1 and IRF3 are necessary but not sufficient to direct IFN-β expression, as they are activated even in cells with low IFN-β expression. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”). Where indicated, the cells were also treated with 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), 10 μM of the TBK1 inhibitor MRT76307 (“TBK1i”), 10 μM of the cGAS inhibitor G140 (“cGASi”), and/or a cocktail of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) at 1:2000 dilution. Protein lysates were probed for phosphorylated IRF3 (Ser396), and β-actin as a loading control. Protein was isolated from treated BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i sample based on tdTomato expression. Western blot for phosphorylated IRF3 for bulk lytic+casp-i treated samples and sorted tdTomato+ and tdTomato- samples were quantified by normalizing the density of phosphorylated protein to unphosphorylated protein bands. Phosphorylation levels are plotted relative to the bulk lytic+casp-i or lytic+casp-i+anti-IFN Abs treated samples. Images shown are representative of 3 replicates. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test.
DOI: 10.6084/m9.figshare.31153444
title: Figure 4K-L primary data

description: Fig 4. TBK1 and IRF3 are necessary but not sufficient to direct IFN-β expression, as they are activated even in cells with low IFN-β expression. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”). Where indicated, the cells were also treated with 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), 10 μM of the TBK1 inhibitor MRT76307 (“TBK1i”), 10 μM of the cGAS inhibitor G140 (“cGASi”), and/or a cocktail of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) at 1:2000 dilution. Protein lysates were probed for phosphorylated IRF3 (Ser396), total IRF3, and β-actin as a loading control. Protein was isolated from treated BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs sample based on tdTomato expression. Western blot for phosphorylated TBK1 and phosphorylated IRF3 for bulk lytic+casp-i+anti-IFN Abs treated samples and sorted tdTomato+ and tdTomato- samples were quantified by normalizing the density of phosphorylated protein to unphosphorylated protein bands. Phosphorylation levels are plotted relative to the bulk lytic+casp-i or lytic+casp-i+anti-IFN Abs treated samples. Images shown are representative of 3 replicates. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test.
DOI: 10.6084/m9.figshare.31153444.v1
title: Figure 4K-L primary data

description: Fig 4. TBK1 and IRF3 are necessary but not sufficient to direct IFN-β expression, as they are activated even in cells with low IFN-β expression. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”). Where indicated, the cells were also treated with 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), 10 μM of the TBK1 inhibitor MRT76307 (“TBK1i”), 10 μM of the cGAS inhibitor G140 (“cGASi”), and/or a cocktail of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) at 1:2000 dilution. Protein lysates were probed for phosphorylated IRF3 (Ser396), total IRF3, and β-actin as a loading control. Protein was isolated from treated BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs sample based on tdTomato expression. Western blot for phosphorylated TBK1 and phosphorylated IRF3 for bulk lytic+casp-i+anti-IFN Abs treated samples and sorted tdTomato+ and tdTomato- samples were quantified by normalizing the density of phosphorylated protein to unphosphorylated protein bands. Phosphorylation levels are plotted relative to the bulk lytic+casp-i or lytic+casp-i+anti-IFN Abs treated samples. Images shown are representative of 3 replicates. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test.
DOI: 10.15468/dl.p7ffvb
title: Occurrence Download

description: A dataset containing 565 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Geometry POLYGON((-53.13269 -24.54746,-53.12169 -24.56959,-53.10257 -24.56696,-53.08403 -24.57012,-53.07187 -24.57275,-53.06434 -24.56748,-53.04812 -24.5659,-53.03653 -24.56379,-53.01973 -24.56696,-53.0122 -24.56696,-52.99134 -24.57328,-52.97396 -24.57328,-52.95832 -24.57012,-52.93921 -24.56379,-52.93399 -24.55536,-52.93168 -24.54483,-52.92762 -24.53534,-52.92009 -24.52849,-52.89055 -24.50688,-52.87722 -24.49844,-52.89255 -24.46001,-52.9143 -24.48257,-52.93706 -24.49775,-52.95021 -24.51156,-52.96488 -24.52813,-52.96892 -24.53595,-52.98814 -24.53963,-53.00028 -24.53871,-53.01191 -24.53733,-53.03366 -24.53457,-53.04934 -24.53457,-53.06552 -24.53687,-53.09485 -24.54055,-53.11053 -24.54147,-53.13269 -24.54746))",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present"
 ]
}

 The dataset includes 565 records from 12 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002532-260129131611470/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.30949245
title: Malignant hilar biliary strictures: palliative drainage during end-of-life care

description: To investigate predictive factors in patients with non-curable malignant hilar biliary obstruction (mHBO) and identify those with a life expectancy of 30 days or less, who would not benefit from palliative biliary drainage. A retrospective analysis of consecutive palliative patients undergoing percutaneous or endoscopic biliary drainage for mHBO at Groote Schuur and Tygerberg Hospitals, Cape Town, between 1 January 2015 and 1 January 2023. Demographic and baseline clinical parameters, laboratory test results, tumour characteristics and intervention type were compared in patients who survived ≤ 30 days to those who survived &gt; 30 days after index intervention. A total of 294 patients were included in the study, of whom 135 survived ≤ 30 days and 159 &gt; 30 days. Regression analysis using a Cox proportional hazard model showed that Eastern Cooperative Oncology Group performance status ≥ 2, strictures secondary to hepatocellular carcinoma, serum levels of albumin &lt; 30 g/L and serum levels of total and conjugated bilirubin &gt; 250 μmol/L predicted survival of ≤ 30 days. These predictive factors should be considered by the multidisciplinary team regarding the decision to perform biliary drainage during end-of-life care or rather proceed to solely medical and symptomatic relief in patients with non-curable mHBO.
DOI: 10.6084/m9.figshare.30949245.v1
title: Malignant hilar biliary strictures: palliative drainage during end-of-life care

description: To investigate predictive factors in patients with non-curable malignant hilar biliary obstruction (mHBO) and identify those with a life expectancy of 30 days or less, who would not benefit from palliative biliary drainage. A retrospective analysis of consecutive palliative patients undergoing percutaneous or endoscopic biliary drainage for mHBO at Groote Schuur and Tygerberg Hospitals, Cape Town, between 1 January 2015 and 1 January 2023. Demographic and baseline clinical parameters, laboratory test results, tumour characteristics and intervention type were compared in patients who survived ≤ 30 days to those who survived &gt; 30 days after index intervention. A total of 294 patients were included in the study, of whom 135 survived ≤ 30 days and 159 &gt; 30 days. Regression analysis using a Cox proportional hazard model showed that Eastern Cooperative Oncology Group performance status ≥ 2, strictures secondary to hepatocellular carcinoma, serum levels of albumin &lt; 30 g/L and serum levels of total and conjugated bilirubin &gt; 250 μmol/L predicted survival of ≤ 30 days. These predictive factors should be considered by the multidisciplinary team regarding the decision to perform biliary drainage during end-of-life care or rather proceed to solely medical and symptomatic relief in patients with non-curable mHBO.
DOI: 10.6084/m9.figshare.30987659
title: Development and validation of a novel clinical decision support tool for sustained remission in Crohn’s disease: a multi-center real-world study

description: Long-term outcomes for Crohn’s disease (CD) patients treated with infliximab (IFX) remain suboptimal. We developed and validated a clinical decision support tool (CDST) to predict sustained remission in CD patients treated with infliximab (IFX). This multicenter observational study analyzed 746 CD patients across three cohorts. Sustained clinical remission (CREM) was defined as steroid-free Crohn’s Disease Activity Index (CDAI) &lt;150 at week 104. Using logistic regression, predictors were weighted by inverse variance. The CDST was internally validated (Cohort I, <i>n</i> = 113) and externally validated (Cohort II, <i>n</i> = 367). Key predictors of CREM included: prior biologic exposure (−18 points), penetrating disease (B3 phenotype, −7 points), albumin (+0.5/gL), younger age (−0.3/year), and absence of antibody to infliximab formation (ATI, +17 points). The model demonstrated strong discrimination (AUC 0.791 [95% CI 0.708–0.875]) and calibration (Brier score: 0.191). External validation AUC was 0.611 (95% CI 0.546–0.675), indicating modest generalizability. Risk stratification <i>via</i> CDST categorized patients into low- (&lt;6 points), intermediate- (6–25), and high-risk (&gt;25) groups. A cutoff of 25 points predicted 2-year CREM with 60% (95%CI 53.2%–66.5%) sensitivity and 52% (95% CI 41.2%–1.8%) specificity. We developed and validated a CDST to identify CD patients likely to achieve sustained remission on IFX therapy. By stratifying patients into distinct risk profiles, it guides personalized therapy initiation and monitoring.
DOI: 10.6084/m9.figshare.30987659.v1
title: Development and validation of a novel clinical decision support tool for sustained remission in Crohn’s disease: a multi-center real-world study

description: Long-term outcomes for Crohn’s disease (CD) patients treated with infliximab (IFX) remain suboptimal. We developed and validated a clinical decision support tool (CDST) to predict sustained remission in CD patients treated with infliximab (IFX). This multicenter observational study analyzed 746 CD patients across three cohorts. Sustained clinical remission (CREM) was defined as steroid-free Crohn’s Disease Activity Index (CDAI) &lt;150 at week 104. Using logistic regression, predictors were weighted by inverse variance. The CDST was internally validated (Cohort I, <i>n</i> = 113) and externally validated (Cohort II, <i>n</i> = 367). Key predictors of CREM included: prior biologic exposure (−18 points), penetrating disease (B3 phenotype, −7 points), albumin (+0.5/gL), younger age (−0.3/year), and absence of antibody to infliximab formation (ATI, +17 points). The model demonstrated strong discrimination (AUC 0.791 [95% CI 0.708–0.875]) and calibration (Brier score: 0.191). External validation AUC was 0.611 (95% CI 0.546–0.675), indicating modest generalizability. Risk stratification <i>via</i> CDST categorized patients into low- (&lt;6 points), intermediate- (6–25), and high-risk (&gt;25) groups. A cutoff of 25 points predicted 2-year CREM with 60% (95%CI 53.2%–66.5%) sensitivity and 52% (95% CI 41.2%–1.8%) specificity. We developed and validated a CDST to identify CD patients likely to achieve sustained remission on IFX therapy. By stratifying patients into distinct risk profiles, it guides personalized therapy initiation and monitoring.
DOI: 10.15468/dl.vz2znh
title: Occurrence Download

description: A dataset containing 41 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Aguapanela arvi"
 ]
}

 The dataset includes 41 records from 3 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002533-260129131611470/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.31153294
title: S5A-C Figure

description: S5 Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. Protein was isolated from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression. Western blots were probed for phosphorylated ATF2, phosphorylated c-Jun, and β-actin as a loading control. Levels of phosphorylated ATF2 and phosphorylated c-Jun in sorted samples were quantified from the western blots, normalized to β-actin, and plotted relative to bulk lytic+casp-i+ anti-IFN Abs samples. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 3.
DOI: 10.6084/m9.figshare.31153294.v1
title: S5A-C Figure

description: S5 Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. Protein was isolated from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression. Western blots were probed for phosphorylated ATF2, phosphorylated c-Jun, and β-actin as a loading control. Levels of phosphorylated ATF2 and phosphorylated c-Jun in sorted samples were quantified from the western blots, normalized to β-actin, and plotted relative to bulk lytic+casp-i+ anti-IFN Abs samples. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 3.
DOI: 10.6084/m9.figshare.31153324
title: S5D Figure

description: S5 Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. RNA was extracted from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression (tdTomato+ and -). mRNA levels of targets of AP-1 – ATF3, GADD45B, and HSPA1A – were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the bulk lytic+casp-i+anti-IFN Abs sample. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153324.v1
title: S5D Figure

description: S5 Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. RNA was extracted from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression (tdTomato+ and -). mRNA levels of targets of AP-1 – ATF3, GADD45B, and HSPA1A – were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the bulk lytic+casp-i+anti-IFN Abs sample. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153330
title: S5E Figure

description: S5E Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. RNA was extracted from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression (tdTomato+ and -). mRNA levels of targets of AP-1 and NF-κB – IL-6 and TNFAIP3 – were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the bulk lytic+casp-i+anti-IFN Abs sample. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153330.v1
title: S5E Figure

description: S5E Fig. AP-1 and NF-κB may be more active in IFN-β high cells. BC3-IFN-βp-tdTomato reporter cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and a cocktail mix of antibodies against type I IFNs and their receptor (“anti-IFN Abs”) to block IFN-β paracrine signaling. RNA was extracted from BC3-IFN-βp-tdTomato reporter cells without sorting (“bulk”), or after sorting the lytic+casp-i+anti-IFN Abs based on tdTomato expression (tdTomato+ and -). mRNA levels of targets of AP-1 and NF-κB – IL-6 and TNFAIP3 – were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the bulk lytic+casp-i+anti-IFN Abs sample. ns = p&gt;0.05, * = p&lt;0.05, ** = p&lt;0.01. One-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153255.v1
title: S4D Figure

description: S4 Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells with stably integrated tdTomato reporters driven by the promoters carrying mutations in the site binding sites for IRF3, NF-κB and AP-1 were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”) and 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). RNA was extracted and tdTomato mRNA levels were measured by RT-qPCR and normalized to 18S rRNA. mRNA levels are plotted relative to the cells containing the WT promoter-driven reporter, lytic+casp-i sample. ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153279
title: S4E Figure

description: S4 Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells with stably integrated tdTomato reporters driven by the promoters carrying mutations in the binding sites for IRF3, NF-κB, AP-1 were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”) and 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). Cells were stained for KSHV ORF45 and analyzed by flow cytometry. ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153279.v1
title: S4E Figure

description: S4 Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells with stably integrated tdTomato reporters driven by the promoters carrying mutations in the binding sites for IRF3, NF-κB, AP-1 were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”) and 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). Cells were stained for KSHV ORF45 and analyzed by flow cytometry. ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 4.
DOI: 10.6084/m9.figshare.31153222
title: S3C Figure

description: S3C Fig. Mitochondrial DNA is the likely cGAS ligand during lytic KSHV infection. BC-3 cells were treated with or without 20 μM dideoxycytidine (“ddC”) for 48 hours to deplete mitochondrial DNA (“mtDNA”), then treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), or vehicle (DMSO, “latent”). At the time of lytic induction, where indicated, the cells were also treated with 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). Cells were stained for KSHV ORF45 and analyzed by flow cytometry. ns = p&gt;0.05, ** = p&lt;0.01, **** = p&lt;0.0001. Two-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 3 for all experiments.
DOI: 10.6084/m9.figshare.31153222.v1
title: S3C Figure

description: S3C Fig. Mitochondrial DNA is the likely cGAS ligand during lytic KSHV infection. BC-3 cells were treated with or without 20 μM dideoxycytidine (“ddC”) for 48 hours to deplete mitochondrial DNA (“mtDNA”), then treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), or vehicle (DMSO, “latent”). At the time of lytic induction, where indicated, the cells were also treated with 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). Cells were stained for KSHV ORF45 and analyzed by flow cytometry. ns = p&gt;0.05, ** = p&lt;0.01, **** = p&lt;0.0001. Two-Way ANOVA followed by Tukey’s post hoc multiple comparisons test for all experiments. n= 3 for all experiments.
DOI: 10.6084/m9.figshare.31153231
title: S4A Figure

description: S4A Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and where indicated, 1 μM of the dual AP-1 and NF-κB inhibitor SP100030. A. RNA was extracted and IFN-β mRNA levels were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the sample treated with TPA, casp-i, and vehicle control (“(-)”). ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 5
DOI: 10.6084/m9.figshare.31153231.v1
title: S4A Figure

description: S4A Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”), 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”), and where indicated, 1 μM of the dual AP-1 and NF-κB inhibitor SP100030. A. RNA was extracted and IFN-β mRNA levels were measured by RT-qPCR, normalized to 18S rRNA, and plotted relative to the sample treated with TPA, casp-i, and vehicle control (“(-)”). ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 5
DOI: 10.6084/m9.figshare.31153255
title: S4D Figure

description: S4 Fig. IFN-β induction during KSHV lytic reactivation requires all three IFN-β enhanceosome transcription factors. BC-3 cells with stably integrated tdTomato reporters driven by the promoters carrying mutations in the site binding sites for IRF3, NF-κB and AP-1 were treated with 20 ng/ml TPA for 48 hours to induce the lytic cycle (“lytic (+TPA)”) and 10 μM of the pan-caspase inhibitor IDN-6556 (“casp-i”). RNA was extracted and tdTomato mRNA levels were measured by RT-qPCR and normalized to 18S rRNA. mRNA levels are plotted relative to the cells containing the WT promoter-driven reporter, lytic+casp-i sample. ns = p&gt;0.05, *** = p&lt;0.001, **** = p&lt;0.0001. Two-Way ANOVA followed by Dunnett’s post hoc multiple comparisons test for all experiments. n= 4.