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MedChemExpress cgas sting pathway activation
Intercellular communication network analysis in tumor microenvironment. (A) Comprehensive cell-cell interaction networks comparing tumor versus normal microenvironments and UNC93B1-dependent signaling contexts. (B) Differential intensity analysis of outgoing and incoming signaling patterns across UNC93B1-dependent cell clusters. (C) Heatmap visualization of UNC93B1-dependent outgoing and incoming signaling patterns. (D) Comparative visualization of pathway activity differences between tumor and normal microenvironments. (E) Differential pathway activity analysis in UNC93B1-dependent subgroups. <t>(F)</t> <t>cGAS-STING</t> signaling interaction networks in tumor versus normal microenvironments. (G) UNC93B1-dependent cGAS-STING signaling interaction networks.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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Intercellular communication network analysis in tumor microenvironment. (A) Comprehensive cell-cell interaction networks comparing tumor versus normal microenvironments and UNC93B1-dependent signaling contexts. (B) Differential intensity analysis of outgoing and incoming signaling patterns across UNC93B1-dependent cell clusters. (C) Heatmap visualization of UNC93B1-dependent outgoing and incoming signaling patterns. (D) Comparative visualization of pathway activity differences between tumor and normal microenvironments. (E) Differential pathway activity analysis in UNC93B1-dependent subgroups. (F) cGAS-STING signaling interaction networks in tumor versus normal microenvironments. (G) UNC93B1-dependent cGAS-STING signaling interaction networks.

Journal: Frontiers in Immunology

Article Title: UNC93B1 promotes pancreatic cancer progression through modulation of cGAS–STING signaling

doi: 10.3389/fimmu.2026.1718849

Figure Lengend Snippet: Intercellular communication network analysis in tumor microenvironment. (A) Comprehensive cell-cell interaction networks comparing tumor versus normal microenvironments and UNC93B1-dependent signaling contexts. (B) Differential intensity analysis of outgoing and incoming signaling patterns across UNC93B1-dependent cell clusters. (C) Heatmap visualization of UNC93B1-dependent outgoing and incoming signaling patterns. (D) Comparative visualization of pathway activity differences between tumor and normal microenvironments. (E) Differential pathway activity analysis in UNC93B1-dependent subgroups. (F) cGAS-STING signaling interaction networks in tumor versus normal microenvironments. (G) UNC93B1-dependent cGAS-STING signaling interaction networks.

Article Snippet: To establish a causal link between UNC93B1 knockdown-induced phenotypes and cGAS-STING pathway activation, rescue experiments were performed using the selective STING inhibitor H-151 (MedChemExpress).

Techniques: Activity Assay

Molecular profiling of cGAS-STING pathway and associated phenotypes following UNC93B1 manipulation. (A–F) Quantitative PCR analysis of key genes in the cGAS-STING pathway (STING, IFN-β, cGAS), cellular senescence marker (p16INK4A), and epithelial-mesenchymal transition regulators (VIM, CDH1) following UNC93B1 knockdown. (*P < 0.05, **P < 0.01, ***P < 0.001).

Journal: Frontiers in Immunology

Article Title: UNC93B1 promotes pancreatic cancer progression through modulation of cGAS–STING signaling

doi: 10.3389/fimmu.2026.1718849

Figure Lengend Snippet: Molecular profiling of cGAS-STING pathway and associated phenotypes following UNC93B1 manipulation. (A–F) Quantitative PCR analysis of key genes in the cGAS-STING pathway (STING, IFN-β, cGAS), cellular senescence marker (p16INK4A), and epithelial-mesenchymal transition regulators (VIM, CDH1) following UNC93B1 knockdown. (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: To establish a causal link between UNC93B1 knockdown-induced phenotypes and cGAS-STING pathway activation, rescue experiments were performed using the selective STING inhibitor H-151 (MedChemExpress).

Techniques: Real-time Polymerase Chain Reaction, Marker, Knockdown

Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations of ADU-S100 and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Journal of Innate Immunity

Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

doi: 10.1159/000550530

Figure Lengend Snippet: Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations of ADU-S100 and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

Techniques: Activation Assay, CCK-8 Assay, Infection, Control

Activation of the STING signaling pathway enhances autophagy in Mtb-infected macrophages. a Western blot analysis of LC3-I to LC3-II conversion in THP-1 cells treated with 4 µ m ADU-S100, 20 µ m HCQ, or si-cGAS for 24 h during Mtb infection. β-actin was used as a loading control. b Densitometric analysis of the LC3-II/β-actin ratio from three independent experiments ( n = 3). ADU-S100 significantly increased LC3-II levels (* p < 0.05). c Representative confocal microscopy images showing the colocalization of Mtb-EGFP (green) and LysoTracker Red-stained lysosomes (red). Nuclei were stained with DAPI (blue). Scale bar = 10 µm. Quantitative analysis is provided in online suppl. Fig. 2. Data in ( b ) are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; *** p < 0.001.

Journal: Journal of Innate Immunity

Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

doi: 10.1159/000550530

Figure Lengend Snippet: Activation of the STING signaling pathway enhances autophagy in Mtb-infected macrophages. a Western blot analysis of LC3-I to LC3-II conversion in THP-1 cells treated with 4 µ m ADU-S100, 20 µ m HCQ, or si-cGAS for 24 h during Mtb infection. β-actin was used as a loading control. b Densitometric analysis of the LC3-II/β-actin ratio from three independent experiments ( n = 3). ADU-S100 significantly increased LC3-II levels (* p < 0.05). c Representative confocal microscopy images showing the colocalization of Mtb-EGFP (green) and LysoTracker Red-stained lysosomes (red). Nuclei were stained with DAPI (blue). Scale bar = 10 µm. Quantitative analysis is provided in online suppl. Fig. 2. Data in ( b ) are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; *** p < 0.001.

Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

Techniques: Activation Assay, Infection, Western Blot, Control, Confocal Microscopy, Staining