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mof
Mof, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sting/diABZI+STING+agonist-1/pm42892943-74-24-31
Average 95 stars, based on 37 article reviews
Mof, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sting/diABZI+STING+agonist-1/pm42892943-74-24-31
Average 95 stars, based on 37 article reviews
mof - by Bioz Stars,
2026-10
95/100 stars
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Western Blot:Article Title: IFI16/204 Promotes Dendritic Cell Activation and Anti-Hepatocellular Carcinoma Efficacy via the STING-TBK1-IRF3 Signalling Pathway. Article Snippet: IFI16 (the murine homologue is IFI204) is an intracellular doublestranded DNA (dsDNA) pattern recognition receptor (PRR) that plays a crucial role in bridging innate and adaptive immunity.. However, its function in dendritic cell (DC) activation and antihepatocellular carcinoma (HCC) efficacy remains poorly characterised.. This study demonstrates that IFI16 promotes DC maturation, functional activation and antitumor immunity. Plasmid Preparation:Article Title: IFI16/204 Promotes Dendritic Cell Activation and Anti-Hepatocellular Carcinoma Efficacy via the STING-TBK1-IRF3 Signalling Pathway. Article Snippet: IFI16 (the murine homologue is IFI204) is an intracellular doublestranded DNA (dsDNA) pattern recognition receptor (PRR) that plays a crucial role in bridging innate and adaptive immunity.. However, its function in dendritic cell (DC) activation and antihepatocellular carcinoma (HCC) efficacy remains poorly characterised.. This study demonstrates that IFI16 promotes DC maturation, functional activation and antitumor immunity. Transfection:Article Title: IFI16/204 Promotes Dendritic Cell Activation and Anti-Hepatocellular Carcinoma Efficacy via the STING-TBK1-IRF3 Signalling Pathway. Article Snippet: IFI16 (the murine homologue is IFI204) is an intracellular doublestranded DNA (dsDNA) pattern recognition receptor (PRR) that plays a crucial role in bridging innate and adaptive immunity.. However, its function in dendritic cell (DC) activation and antihepatocellular carcinoma (HCC) efficacy remains poorly characterised.. This study demonstrates that IFI16 promotes DC maturation, functional activation and antitumor immunity. Activation Assay:Article Title: IFI16/204 Promotes Dendritic Cell Activation and Anti-Hepatocellular Carcinoma Efficacy via the STING-TBK1-IRF3 Signalling Pathway. Article Snippet: IFI16 (the murine homologue is IFI204) is an intracellular doublestranded DNA (dsDNA) pattern recognition receptor (PRR) that plays a crucial role in bridging innate and adaptive immunity.. However, its function in dendritic cell (DC) activation and antihepatocellular carcinoma (HCC) efficacy remains poorly characterised.. This study demonstrates that IFI16 promotes DC maturation, functional activation and antitumor immunity. other:Article Title: Irradiation combined with PD-L1 −/− and autophagy inhibition enhances the antitumor effect of lung cancer via cGAS-STING-mediated T cell activation Article Snippet: In some experiments, LLC cells were pre-treated with 25 μM chloroquine (CQ, an inhibitor of autophagy) or 20 μM Article Title: A biomimetic arsenic-based nanozyme enhances dual epigenetic regulation to improve the efficacy of immunotherapy for acute myeloid leukaemia. Article Snippet: Aberrant epigenetic modifications in acute myeloid leukaemia (AML) limit immunotherapeutic efficacy.. Arsenic ions are capable of undergoing valence transformation in organisms, exhibit favourable enzyme-mimetic activity, and thereby play a crucial role in enhancing dual epigenetic regulation.. Therefore, to achieve potent epigenetic regulation, in this study, a biomimetic arsenic-based nanozyme (As/ZIF-8@M) that exhibits leukaemia cell recognition and phagocytosis capabilities, as well as bone marrow homing effects, was engineered. Incubation:Article Title: IQGAP1 promotes mitochondrial damage and activation of the mtDNA sensor cGAS-STING pathway to induce endothelial cell pyroptosis leading to atherosclerosis. Article Snippet: Atherosclerosis (AS) is the most common cardiovascular disease and has limited therapeutic options.. IQ motifcontaining GTPase-activating protein 1 (IQGAP1) is an important scaffolding protein regulating mitochondrial function influencing endothelial cell activity.. Evidence suggests that mitochondrial damage can lead to leakage of mtDNA into the cytoplasm to activate the DNA sensor cGAS-STING to mediate pyroptosis. Cell Culture:Article Title: IQGAP1 promotes mitochondrial damage and activation of the mtDNA sensor cGAS-STING pathway to induce endothelial cell pyroptosis leading to atherosclerosis. Article Snippet: Atherosclerosis (AS) is the most common cardiovascular disease and has limited therapeutic options.. IQ motifcontaining GTPase-activating protein 1 (IQGAP1) is an important scaffolding protein regulating mitochondrial function influencing endothelial cell activity.. Evidence suggests that mitochondrial damage can lead to leakage of mtDNA into the cytoplasm to activate the DNA sensor cGAS-STING to mediate pyroptosis. Purification:Article Title: Glycyrrhetinic acid blocks SARS-CoV-2 infection by activating the cGAS-STING signalling pathway. Article Snippet: Hebei Academy of Integrated Traditional Chinese and Western Medicine, Shijiazhuang, Hebei, China State Key Laboratory for Innovation and Transformation of Luobing Theory, Shijiazhuang, China New Drug Evaluation Center, Shijiazhuang Yiling Pharmaceutical Co., Ltd, Shijiazhuang, Hebei, China State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China Injection:Article Title: MLKL Deficiency Attenuated Hepatocyte Oxidative DNA Damage by Activating Mitophagy to Suppress Macrophage cGAS-STING Signaling During Liver Ischemia and Reperfusion Injury. Article Snippet: In vitro, primary hepatocytes were prepared and transiently transfected with PINK1 small interfering RNA (siRNA) or control siRNA (GeneChem, China) using Lipofectamine 3000 (Thermo Fisher Scienti c, USA). .. |
![(A) Kinetics of 2′3′- 32 [P]-cGAMP degradation by tissue lysates from the indicated CNS regions of WT mice at 10 weeks of age (n=2 biological replicates). (B, C) mRNA expression levels of Enpp1 in whole brain (B) and spinal cord (C) tissue of WT healthy (n=3 biological replicates) and MOG 35-55 -induced EAE mice at the symptomatic phase (paralysis score ≥ 2) (n=3 biological replicates). (D) Representative thin layer chromatography (TLC) tracking 2′3′- 32 [P]-cGAMP degradation by spinal cord lysate of WT healthy and EAE mice (paralysis score ≥ 2), at the indicated timepoints. (E) Kinetics of 2′3′- 32 [P]-cGAMP degradation by the spinal cord lysate of healthy and EAE mice (n=2 biological replicates). (F) 2′3′-cGAMP levels in healthy (n=3 biological replicates) and EAE (n=4 biological replicates) brain and spinal cord tissue measured by enzyme-linked immunosorbent assay (ELISA). (G) mRNA expression levels of Cxcl10 and Il1b in whole brain and spinal cord tissue of WT healthy (n=3) and MOG 35-55 -induced EAE mice (n=3) mice. (H, I) Expression of Enpp1 in microglia (H), oligodendrocyte precursor cells (OPCs), and committed oligodendrocyte precursors (COPs) (I) across the indicated MS diagnoses compared to healthy donors. Legends: CTRL : control; SPMS : secondary progressive MS; PPMS : primary progressive MS. (EGA: EGAD00001009169). Data are mean ± s.e.m. p -values were calculated using Mann-Whitney t-test. (J) Kinetics of 2′3′- 32 [P]-cGAMP degradation by tissue lysates of the indicated CNS regions of Enpp1 H362A mice at 10 weeks of age (n=2 biological replicates). (K) Paralysis scores for WT, Enpp1 H362A , and Enpp1 H362A <t>Sting</t> gt/gt mice at the indicated times after MOG 35-55 immunization. Number of mice in each group is indicated in the legend. Significance calculated by two-way ANOVA. (I) Paralysis scores in WT mice treated with cGAS inhibitor RU.521 after EAE onset (n= 14 mice for vehicle and n=17 mice for RU.521 treatment). Data was pooled from 2 independent experiments. Significance of the treatment course was calculated by two-way ANOVA and significance of daily score was calculated by two-sided unpaired t-test with Welch’s correction. (M) Experimental scheme to measure mitochondrial DNA leakage in different cell types of the spinal cord during EAE symptomatic phase: spinal cord tissue single cell dissociation, followed by FACS, subcellular fractionation, and qPCR of mitochondrial genes. (N) Cytosolic mtDNA (mt-ND1) in CD11b + CD45 lo microglia, CD11b + CD45 hi macrophages, CD3 + T cells, CD45 − non-immune cells isolated from WT healthy and EAE mice, normalized to total mt-ND1 DNA in the heavy fraction (n=4 biological replicates per group). (O,P) Cytosolic mtDNA (mt-ND1) normalized to total MT-ND1 DNA (O) or total genomic DNA (B2M) (P) in the heavy fraction of MACS-sorted mouse primary spinal cord macrophages (CD11b + ) from WT mice at 10 weeks of age, with or without MOG 35-55 -induced EAE (n=3-4 biological replicates per group). (Q) 2′3′-cGAMP secretion by MACS-sorted mouse primary brain and spinal cord macrophages (CD11b + ) from wild-type mice with or without MOG 35-55 -induced EAE. Cells were cultured for 5 days after sorting and incubated for 48 h in the presence of ENPP1 inhibitor STF-1623. 2′3′-cGAMP levels in the supernatant were measured by enzyme-linked immunosorbent assay (ELISA) (n=5 biological replicates). Data are mean ± s.e.m. p -values were calculated using unless otherwise indicated.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_37/10__64898_slash_2026__09__30__754737/10__64898_slash_2026__09__30__754737___F1.large.jpg)
![(A) MACS-sorted CD11b + primary mouse brain microglia from aged wild-type mice were incubated for 48 h in the presence of ENPP1 inhibitor STF-1623. Supernatant was concentrated by solid-phase extraction with aminopropyl columns and 2′3′-cGAMP levels were measured by enzyme-linked immunosorbent assay (ELISA) and normalized to total protein amount in the cell lysates (n=8 biological replicates). (B) Differential gene expression from bulk RNA-seq analysis of young and aged mice forebrains (n=2 biological replicates per group). The volcano plot shows bolded type I IFN and inflammatory from the total list of DEGs (adjusted p-value ≤ 0.05, |[fold change (FC)]| ≥ 1.5). (C) Functional enrichment sorted on adjusted p -value in ascending order. Pathways identified with gene set enrichment analysis (GSEA) using the Hallmark gene set reveal interferon response as the top-enriched pathway in bulk RNA-seq analysis of young and aged mice forebrains (n=2 biological replicates per group). (D,E) Relative transcript levels of type I IFN and interferon-stimulated genes (ISGs) in whole brain tissue (D) and spinal cord tissue (E) of wild-type mice at 10 weeks of age (young) and 22–24 months of age (aged) (n=4–5 mice per group). (F) Kinetics of 2′3′-cGAMP degradation by different CNS regions of Enpp1 H362A mice at 22 months of age (n=2 biological replicates). (G) Strategy to assess the effect of extracellular cGAMP on aging-related neurodegeneration. (H, I) Average latency to fall (H) and average speed at fall (I) across three consecutive trials at the accelerating rotarod test with wild-type (n=6–17 per age group), Enpp1 H362A (n=6–32 per age group), and Enpp1 H362A Sting gt/gt (n=6–15 per age group) (n=3–6 independent experiments performed for different age groups). (J,K,L) Time to turn (TTT), time to descend (TTD), and percentage of failed trials in the pole across three consecutive trials with wild-type (n=8), Enpp1 H362A (n=9 mice per age group), and Enpp1 H362A Sting gt/gt (n=9 mice per age group) mice at 4–6 months of age (n=2 independent experiments). (M) Time spent at the center during open field testing of wild-type (n=10–13 per age group), Enpp1 H362A (n=11–16) and Enpp1 H362A Sting gt (n=9–13) mice at 4 and 22 months of age. Data are mean ± s.e.m. p -values were calculated using two-sided unpaired t-test with Welch’s correction unless otherwise indicated.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_37/10__64898_slash_2026__09__30__754737/10__64898_slash_2026__09__30__754737___F2.large.jpg)
![(A) Representative thin layer chromatography (TLC) tracking 2′3′- 32 [P]-cGAMP degradation by tissue lysates from the indicated CNS regions of Enpp1 H362A mice at 22–24 months of age (n=2 biological replicates). (B,C) Relative transcript levels of the indicated ISGs in whole brain tissue (A) and spinal cord tissue (B) of WT (n=3–4) and Enpp1 H362A (n=4–5) mice at 22–24 months of age. (D,E) mRNA expression levels of Cxcl10 (D) and Il1b (E) at the indicated CNS regions of WT, Enpp1 H362A , and Enpp1 H362A Sting gt/gt mice at 4–6 months of age. (F) Body weights of WT, Enpp1 H362A and Enpp1 H362A Sting gt/gt mice at 22–24 months of age. Only mice weighing between 25–35 g underwent accelerating rotarod and pole testing. (G) Discrimination index during the novel object recognition test (NOR) for WT, Enpp1 H362A and Enpp1 H362A Sting gt/gt mice (n=6 mice per group). Only successfully completed tests are plotted. n.a. stands for not applicable, which we used for mice from the Enpp1 H362A genotype that did not interact with either object. (H) Time to reach 30 s of total exploration during the novel object recognition test (NOR) for WT, Enpp1 H362A , and Enpp1 H362A Sting gt/gt mice at 22–24 months of age. The failure threshold of 600s denotes the total duration of the experiment, and 800s denotes the total time of recording (n=6 mice per genotype). (I-K) Distance moved (I), average velocity (J), and time spent at walls (K) during open field testing of WT (n=13), Enpp1 H362A (n=16) and Enpp1 H362A Sting gt/gt (n=13) mice at 22–24 months of age. (L-N) Distance moved (L), average velocity (M), and time spent at walls (N) during open field testing of WT (n=10), Enpp1 H362A (n=11) and Enpp1 H362A Sting g/gtt (n=9) mice at 22–24 months of age. Data are mean ± s.e.m. p -values were calculated using two-sided unpaired t-test with Welch’s correction unless otherwise indicated.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_37/10__64898_slash_2026__09__30__754737/10__64898_slash_2026__09__30__754737___F7.large.jpg)
