Journal: Human Mutation

Article Title: PLSCR3 Deficiency Triggers mtDNA‐Driven cGAS‐STING Activation to Potentiate Antitumor Immunity in Colorectal Cancer

doi: 10.1155/humu/8545428

Figure Lengend Snippet: PLSCR3 deficiency activates mtDNA‐associated cGAS‐STING signaling. (A) 2 ′ ‐3 ′ ‐cGAMP quantification by ELISA in PLSCR3 knockdown (KD_PLSCR3) HT29 cells and normal controls (NCs) treated with Scramble or dideoxycytidine (DDC) ( p < 0.0001; ns = not significant; n = 3). (B, C) KD_PLSCR3 cells exhibited an elevation in IFN β and CXCL10 production measured by ELISA compared to NC ( p < 0.0001, n = 3). CRISPR‐mediated STING knockout (STING sg) completely abrogated these effects. (D) Western blot analysis showed upregulation of phosphorylated STING and innate immune effectors (IFIH1, ISG60, and ISG15 protein) in STING‐competent KD_PLSCR3 cells relative to GAPDH loading controls. (E) Normalized mRNA level quantification by qPCR demonstrated significant induction of interferon‐stimulated genes (ISGs) in STING‐competent KD_PLSCR3 cells compared with the other groups. Data in panels A–C and E are presented as mean ± SD. Statistical significance was determined using one‐way ANOVA followed by Tukey′s multiple‐comparisons post hoc test for multiple‐group comparisons.

Article Snippet: STING agonist (Cat. No. HY‐103665, CAS No.: 2138299‐29‐1) and DDC (Cat. No. HY‐17392, CAS No.: 7481‐89‐2) were purchased from MedChemExpress (Shanghai, China).

Techniques: Enzyme-linked Immunosorbent Assay, Knockdown, CRISPR, Knock-Out, Western Blot

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: WT and Tlr9–/– mice were subjected to CLP. PLF was collected at 18 hours after CLP. (A) Percentages of indicated immune cells were measured by flow cytometry. (B) TLR9 expression in indicated peritoneal cells. MFI for TLR9 expression was measured by flow cytometry. (C–G) Peritoneal cell counts of (C) B cells, (D) macrophages, (E) DCs, (F) neutrophils, and (G) T cells in control and after CLP. Data are shown as mean ± SD from 2 separate experiments. Symbols represent individual mice. *P < 0.05; **P < 0.01; ***P < 0.001, unpaired, 2-tailed Student’s t tests.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Flow Cytometry, Expressing

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: (A–D) WT and Tlr9–/– mice were subjected to CLP. Plasma and PLF were collected at 18 hours after CLP. (A) Peritoneal B-1 cell numbers. (B) Plasma IgM levels. (C) Peritoneal IgM levels. (D) Peritoneal GM-CSF levels. (E–G) Tlr9–/– mice were treated with CD19 neutralizing antibodies (10 mg/mouse) or control IgG (10 mg/mouse) at 24 hours before CLP. PLF was collected at 18 hours after CLP. (E) Seven-day survival after CLP. Data are from 2 separate experiments. n = 10. *P < 0.05, log-rank test. (F) Bacterial clearance in PLF. Data are from 2 separate experiments. Symbols represent individual mice. *P < 0.05, nonparametric Mann-Whitney U test. (G) Peritoneal IgM levels. For A–D and G, data are shown as mean ± SD from 2 separate experiments. Symbols represent individual mice. *P < 0.05; **P < 0.01; ***P < 0.001, unpaired, 2-tailed Student’s t test.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: MANN-WHITNEY

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: (A) WT and Tlr9–/– mice were subjected to CLP. PLF was collected at 18 hours after CLP. Peritoneal CXCL13 levels were assessed using ELISA. (B–F) WT and Tlr9–/– mice were treated with CXCL13 neutralizing antibodies (10 mg/mouse) or control IgG (10 mg/mouse) immediately after CLP. PLF and plasma were collected at 18 hours after CLP. (B) Peritoneal B-1 cell numbers. (C) Peritoneal IgM levels. (D) Bacterial load in PLF. (E) Plasma IL-6 levels. (F) Seven-day survival. For A–C and E, data are shown as mean ± SD. Symbols represent individual mice. *P < 0.05; **P < 0.01, unpaired, 2-tailed Student’s t tests. For D, symbols represent individual mice. *P < 0.05, nonparametric Mann-Whitney U test. For F, n = 13–19/group as indicated. *P < 0.05 versus Tlr9–/– IgG, log-rank test. (G–K) WT mice were treated with recombinant CXCL13 (10 mg/mouse) or PBS immediately after CLP. (G) Peritoneal B-1 cell number. (H) Peritoneal IgM levels. (I) Bacterial load in PLF. (J) Plasma IL-6 levels. (K) Seven-day survival. For G, H, and J, data are shown as mean ± SD. Symbols represent individual mice. *P < 0.05, unpaired, 2-tailed Student’s t test. For I, symbols represent individual mice. *P < 0.05, nonparametric Mann-Whitney U test. For K, n = 10/group. *P < 0.05, log-rank test.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Recombinant

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: (A–C) WT and Tlr9–/– mice were subjected to CLP. PLF and mesenteric adipose tissue were collected at18 hours after CLP. (A and B) Cxcl13 expression in peritoneal cells (A) and mesenteric adipose tissue (B) were assessed using quantitative PCR. Data are shown as mean ± SD from 2 separate experiments. Symbols represent individual mice. *P < 0.05, 2-tailed Student’s t test. (C) Immunofluorescence staining of CXCL13 (red), CD45 (green), CD11c (white), and nucleus (blue) in mesenteric adipose tissue. Scale bar: 5 μm. (D and E) Cxcl13 expression in mouse FRCs. WT and Tlr9–/– FRCs were isolated from mesenteric adipose tissues and expanded ex vivo. FRCs were stimulated with indicated TLR ligands (ODN1585, 5 μM; ODN1826, 5 μM; ODN2395, 5 μM, LPS, 1 μg/mL; PIC, 20 μg/mL) for 18 hours. Cxcl13 expression was assessed using quantitative PCR. Data are shown as mean ± SD from 1 representative experiment. Experiments were performed 3 times. *P < 0.05; **P < 0.01; ***P < 0.001, 1-way ANOVA with Bonferroni’s post hoc analysis.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Expressing, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Isolation, Ex Vivo

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: (A) Schematic timeline of experimental set and analysis for adoptive transfer studies. (B and C) Mice were subjected to CLP. WT or Tlr9–/– FRCs (2 × 105/ mouse) were injected i.p. at 1 hour after CLP. (B) Bacterial load in PLF at 18 hours after CLP. (C) Circulating IL-6 levels at 18 hours after CLP. Data are shown as mean ± SD from 2 separate experiments. *P < 0.05, unpaired, 2-tailed Student’s t test. (D and E) Seven-day survival. (D) Mice were subjected to CLP. PBS, WT, or Tlr9–/– FRCs (2 × 105/ mouse) were injected i.p. 1 hour after CLP. n = 13 in PBS group; n = 19 in WT FRC group; n = 22 in Tlr9–/– FRC group. (E) Mice were subjected to CLP. PBS, WT, or Tlr9–/– FRCs (2 × 105/ mouse) were injected i.p. at 12 hours after CLP. n = 10 in PBS group; n = 14 in WT FRC group; n = 15 in Tlr9–/– FRC group. *P < 0.05 vs. PBS, log-rank test. Data are from 3 separate experiments for D and 2 separate experiments for E. Statistical differences were determined using the log-rank test.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Adoptive Transfer Assay, Injection

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: Human FRCs were isolated from adipose tissue and expanded ex vivo. (A) TLR9 expression in human FRCs. TLR9 expression was assessed using flow cytometry. Numbers indicate percentage of FRCs (CD45–CD31–PDPN+). (B) Chemokine expression in human FRCs. FRCs were stimulated with indicated TLR ligands (ODN2216, 5 μM; LPS, 1 μg/mL; PIC, 20 μg/mL) for 18 hours. Indicated chemokine expression was assessed using quantitative PCR. Data are shown as mean ± SD from 1 representative experiment. Experiments were performed 3 times. *P < 0.05; **P < 0.01; ***P < 0.001, 1-way ANOVA with Bonferroni’s post hoc analysis.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Isolation, Ex Vivo, Expressing, Flow Cytometry, Real-time Polymerase Chain Reaction

Journal: The Journal of Clinical Investigation

Article Title: TLR9 signaling in fibroblastic reticular cells regulates peritoneal immunity

doi: 10.1172/JCI127542

Figure Lengend Snippet: Activation of TLR9 signaling in FRCs suppresses the production of chemokines, which are essential for recruiting B cells, T cells, macrophages, and neutrophils into the peritoneal cavity as well as driving the formation of FALCs.

Article Snippet: LPS-EK (LPS from E . coli K12), PIC low molecular weight (LMW), Mouse TLR9 Agonist Kit, and Human TLR9 Agonist Kit were purchased from InvivoGen.

Techniques: Activation Assay

Journal: Cell reports

Article Title: AAV5-mediated manipulation of insulin expression in choroid plexus has long-term metabolic and behavioral consequences

doi: 10.1016/j.celrep.2023.112903

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: ​ REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Monoclonal Rabbbit anti-TTR (prealbumin) AbCam Cat # ab75815; RRID:AB_1310604 Monoclonal Rabbit anti-Insulin Cell Signaling Cat # 3014; RRID:AB_2126503 Polyclonal Rabbit anti-mCherry Rockland Cat # 600-401-P16; RRID:AB_2614470 Monoclonal Rabbit anti- p -Akt (Ser473) Cell Signaling Cat # 4060; RRID:AB_2315049 Monoclonal Mouse anti-Alpha1 Na+/K+ ATPase AbCam Cat # ab7671; RRID:AB_306023 Bacterial and virus strains AAV5-CMV-CRE Vector Biolabs Cat # 7012 AAV5-CMV-GFP Vector Biolabs Cat # 7006 AAV5-CMV-Ins2 Vector Biolabs Cat # AAV-262269 AAV5-CMV-GCaMP6f Vector Biolabs Built to order AAV5-TTR-hM3Dq-mCherry Vector Biolabs Built to order AAV5-CMV-Psck1 Vector Biolabs Cat # AAV-268239 AAV5-CMV-Pcsk2 Vector Biolabs Cat # AAV-268242 Chemicals, peptides, and recombinant proteins Compound 21 TOCRIS Cat # 5548 Critical commercial assays PicoPure RNA Isolation Kit ThermoFisher Cat # KIT0204 Ultra Sensitive Insulin ELISA Kit CrystalChem Cat # 90080 Deposited data Raw and analyzed data of RNA-seq This paper GEO: GSE218188 Experimental models: Cell lines iPS(IMR90)-4 WiCell WISCi004-B Experimental models: Organisms/strains C57BL/6J The Jackson Laboratory Strain # 000664 Ai14 The Jackson Laboratory Strain #007914 Ins1 −/− Ins2 fl/fl This paper N/A Software and algorithms ImageJ NIH https://imagej.nih.gov/ij/ GraphPad Prism GraphPad https://graphpad.com R R Foundation for Statistical Computing https://www.r-project.org Other Normal chow diet Dyets Inc Cat# 101845 High fat/high sugar diet Dyets Inc Cat# 103806 Open in a separate window KEY RESOURCES TABLE.

Techniques: Virus, Plasmid Preparation, Recombinant, Isolation, Enzyme-linked Immunosorbent Assay, Software

Journal: Cell Communication and Signaling : CCS

Article Title: STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury

doi: 10.1186/s12964-026-02830-2

Figure Lengend Snippet: ZBP1 deficiency alleviates PANoptosis induced by STING agonism. A ZBP1 mRNA levels (fold change) in primary tubular epithelial cells (PRTCs) treated with diABZI (STING agonist, 10 µM) for 6, 12, and 24 h (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001. B ZBP1 mRNA levels (fold change) PRTCs treated with DMSO or diABZI in STING+/+-PRTCs and STING-/-- PRTCs (n = 3). *P < 0.05 ，**P < 0.01，***P <0.001. C Western blots and quantification of STING and ZBP1 protein PRTCs treated with DMSO or diABZI in STING+/+-PRTCs and STING-/-- PRTCs (n = 3). *P < 0.05 ，**P < 0.01，***P <0.001. D Immunofluorescence of ZBP1 (red), STING (green), and DAPI (blue) in PRTCs treated with diABZI (scale bars: 40 μm), The figure on the right is an enlarged view of the area within the white dashed box in the left one. E Inflammation markers: TNFα, IL1β mRNA levels and Cell viability assay with LDH release and Cell Viability Assay in ZBP1+/+-PRTCs and ZBP1-/--PRTCs treated with DMSO or diABZI (n = 4). *P < 0.05 ，**P < 0.01，***P <0.001. F Western blot analysis of PANoptosis markers (pyroptosis: GSDMD, N-GSDMD; apoptosis: CAS3, c-CAS3, CAS7, c-CAS7; necroptosis: p-RIP1, p-MLKL) in ZBP1+/+-PRTCs and ZBP1-/--PRTCs treated with DMSO or diABZI (n=3; α-Tubulin loading control). Red separator lines indicate different experimental conditions. G Flow cytometry quantification of cell death counts (PI+, V610) in ZBP1+/+-PRTCs and ZBP1-/--PRTCs treated with DMSO or diABZI (n=3)

Article Snippet: Primary cells were treated with diABZI (medchemexpress-HY-112921A), Cocl2 (sigma-232696), Fludarabine (medchemexpress-HY-B0069), Anifrolumab (medchemexpress-HY- P99168 ), IFN-α (medchemexpress-HY-P7023), Necrostatin-1 (medchemexpress-HY-15760), Z-VAD-FMK (medchemexpress-HY-16658B), MCC950 (medchemexpress-HY-12815), 2’3’-cGAMP (c-GAMP: tlrl-nacga23-02) for 24–48 h.

Techniques: Western Blot, Immunofluorescence, Viability Assay, Control, Flow Cytometry

Journal: Cell Communication and Signaling : CCS

Article Title: STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury

doi: 10.1186/s12964-026-02830-2

Figure Lengend Snippet: STING induces ZBP1 activation in a STAT1-dependent manner. A Immunofluorescence of STAT1 (red), STING (green), and DAPI (blue) in renal cortices from STINGflox/flox-Sham, STINGflox/flox-IR, STINGCKO-Sham, and STINGCKO -IR groups, with quantification showing STING-dependent STAT1 upregulation during injury (n=5, scale bars: 50 μm). B Western blot confirmation of STAT1 and p-STAT1 protein expression trends in vivo (n=3; α-Tubulin loading control). C Nucleocytoplasmic fractionation in primary renal tubular epithelial cells (PRTCs) treated with PBS, 2’3’cGAMP (c-GAMP, 2 μg/ml), diABZI (10 μM), or H/R, revealing STAT1 and p-STAT1 nuclear accumulation upon STING activation (Lamin B/α-Tubulin: compartment markers). D Immunofluorescence confirming diABZI-driven STAT1 nuclear translocation in PRTCs (STAT1: red; DAPI: blue) (scale bars: 20 μm). E Confocal immunofluorescence microscopy images of PRTCs treated with diABZI, stained for STAT1 (red), STING (green), and DAPI (blue) (scale bars: 20 μm); a magnified detail of the white-boxed area is shown in the inset. The panel shows fluorescence co-localization analysis using the Plot Profile function in ImageJ-Fiji. F Molecular docking (GRAMM/HDOCK) predicted contact sites between STING (violet) and STAT1 (celeste); a magnified detail of the yellow-boxed area is shown in the inset. The black arrows represent the predicted hydrogen bonding. G Co-immunoprecipitation (Co-IP) of STING and STAT1 from PRTCs using antibodies against STAT1 and STING. Input: whole-cell lysate; IgG: negative control. H WT (HA-STING-WT) or mutant STING (HA-STING-CTD) expression vectors were cotransfected with Flag tagged STAT1 into 293T cells, and cell lysis was used for IP with anti-HA, followed by Western blot detection of STING or STAT1. I The schematic diagram of truncated plasmid of STING

Article Snippet: Primary cells were treated with diABZI (medchemexpress-HY-112921A), Cocl2 (sigma-232696), Fludarabine (medchemexpress-HY-B0069), Anifrolumab (medchemexpress-HY- P99168 ), IFN-α (medchemexpress-HY-P7023), Necrostatin-1 (medchemexpress-HY-15760), Z-VAD-FMK (medchemexpress-HY-16658B), MCC950 (medchemexpress-HY-12815), 2’3’-cGAMP (c-GAMP: tlrl-nacga23-02) for 24–48 h.

Techniques: Activation Assay, Immunofluorescence, Western Blot, Expressing, In Vivo, Control, Fractionation, Translocation Assay, Microscopy, Staining, Fluorescence, Immunoprecipitation, Co-Immunoprecipitation Assay, Negative Control, Mutagenesis, Lysis, Plasmid Preparation

Journal: Cell Communication and Signaling : CCS

Article Title: STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury

doi: 10.1186/s12964-026-02830-2

Figure Lengend Snippet: STING Drives STAT1-Mediated Transcriptional Activation of ZBP1 to Promote PANoptosis. A Using CUT-Tag assays in HK-2 cells treated with diABZI, isolated DNA fragments bound to STAT1 and identified potential binding sites on the ZBP1 promoter via Jaspar website. B Exploration of STAT1-ZBP1 promoter binding in diABZI-treated HK-2 cells: ZBP1 promoter region amplified using Primer3Plus-designed primers, Cleavage Under Targets and Tagmentation with STAT1 antibody compared with IgG control (n=3). C Western blot confirmation of ZBP1 and p-STAT1 protein expression trends in PRTCs treated with DMSO, diABZI, Fludarabine and diABZI groups (n=3; α-Tubulin loading control). D - E Fludarabine (STAT1 inhibitor) suppresses diABZI-induced ZBP1 mRNA and protein (n=4 mRNA, n=3 protein) and inflammatory cytokines (TNFα, IL1β mRNA; n=4) in PRTCs (*P<0.05, **P<0.01, ***P<0.001). F Viability assessment by PI (red, dead cells)/Calcein-AM (green, live cells) staining in PRTCs treated with DMSO, diABZI or diABZI and Fludarabine (n=3, scale bars: 50 μm). G PRTCs were treated with DMSO (control), diABZI (STING agonist), or diABZI and Fludarabine. Flow cytometry quantification of cell death (PI⁺, V610). H Western blot analysis of PANoptosis markers (pyroptosis: GSDMD, N-GSDMD; apoptosis: CAS3, c-CAS3, CAS7, c-CAS7; necroptosis: p-RIP1, p-MLKL) in PRTCs treated with DMSO, diABZI or diABZI and Fludarabine (n=3, α-Tubulin loading control)

Article Snippet: Primary cells were treated with diABZI (medchemexpress-HY-112921A), Cocl2 (sigma-232696), Fludarabine (medchemexpress-HY-B0069), Anifrolumab (medchemexpress-HY- P99168 ), IFN-α (medchemexpress-HY-P7023), Necrostatin-1 (medchemexpress-HY-15760), Z-VAD-FMK (medchemexpress-HY-16658B), MCC950 (medchemexpress-HY-12815), 2’3’-cGAMP (c-GAMP: tlrl-nacga23-02) for 24–48 h.

Techniques: Activation Assay, Isolation, Binding Assay, Amplification, Control, Western Blot, Expressing, Staining, Flow Cytometry

Journal: Cell Communication and Signaling : CCS

Article Title: STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury

doi: 10.1186/s12964-026-02830-2

Figure Lengend Snippet: STING and IFNAR Pathways Cooperatively Promote STAT1 Activation Drives PANoptosis in Renal Tubular Epithelial Cells . A - B Primary renal tubular epithelial cells (PRTCs) were treated with DMSO (control), diABZI (STING agonist), or diABZI and Anifrolumab (IFNAR inhibitor). Representative Western blot analysis and quantification of PANoptosis markers (pyroptosis: GSDMD, N-GSDMD; apoptosis: CAS3, c-CAS3, CAS7, c-CAS7; necroptosis: p-RIP1, p-MLKL) and ZBP1 in PRTCs (n=3 α-Tubulin loading control). Red separator lines indicate different experimental conditions. C Primary renal tubular epithelial cells (PRTCs) were treated with DMSO, diABZI, or diABZI and Anifrolumab. Flow cytometry quantification of cell death (PI⁺, V610). D - E PRTCs were treated with DMSO, diABZI, or diABZI (10 μM) and IFN-α (1 ng/ml). Western blot analysis and quantification of PANoptosis markers (pyroptosis: GSDMD, N-GSDMD; apoptosis: CAS3, c-CAS3, CAS7, c-CAS7; necroptosis: p-RIP1, p-MLKL) in each group (n=3; α-Tubulin loading control). Red separator lines indicate different experimental conditions. F Proposed mechanism of the STING-STAT1-ZBP1 axis in renal tubular epithelial cells promoting pan-apoptosis in IRI-AKI. Following IRI-AKI, STING interacts with and activates STAT1, facilitating its nuclear translocation. STAT1 binds to the promoter region of the ZBP1 gene, initiating its transcription. The upregulated ZBP1 subsequently triggers the activation of PANoptosis, which drives the progression of AKI

Article Snippet: Primary cells were treated with diABZI (medchemexpress-HY-112921A), Cocl2 (sigma-232696), Fludarabine (medchemexpress-HY-B0069), Anifrolumab (medchemexpress-HY- P99168 ), IFN-α (medchemexpress-HY-P7023), Necrostatin-1 (medchemexpress-HY-15760), Z-VAD-FMK (medchemexpress-HY-16658B), MCC950 (medchemexpress-HY-12815), 2’3’-cGAMP (c-GAMP: tlrl-nacga23-02) for 24–48 h.

Techniques: Activation Assay, Control, Western Blot, Flow Cytometry, Translocation Assay