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    Cell Signaling Technology Inc p tbk1
    COPN mitigates retinal ischemia‒reperfusion injury by suppressing the <t>cGAS–STING–TBK1</t> signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
    P Tbk1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1606 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+tbk1/Phospho-TBK1%2FNAK+(Ser172)+XP+Rabbit+mAb/pmc13049686-160-60-61
    Average 98 stars, based on 1606 article reviews
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    1) Product Images from "A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation"

    Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

    Journal: Materials Today Bio

    doi: 10.1016/j.mtbio.2026.102974

    COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
    Figure Legend Snippet: COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Techniques Used: Quantitative Proteomics, Control, Activation Assay, Phospho-proteomics, Disruption, Western Blot

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    Activity Assay:

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells.
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 ◦C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 °C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Binding Assay:

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells.
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 ◦C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 °C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Incubation:

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells.
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 ◦C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Article Title: Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells
    Article Snippet: .. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide for 10 min, and nonspecific binding was reduced by incubation with 5% bovine serum albumin (BSA) for 1 h. Sections were then incubated overnight at 4 °C with primary antibodies targeting Ki67 (1:200, CST, Cat# 9027), STING (1:200, CST, Cat# 13647), p-TBK1 (1:200, CST, Cat# 5483), and p-IRF-3 (1:200, CST, Cat# 4947). ..

    Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation
    Article Snippet: .. The following primary antibodies were used: Drp1 (CST, #8570, 1:1000, ∼80 kDa), Fis1 (Proteintech, 10956-1-AP, 1:1000, ∼17 kDa), Mfn1 (Abcam, ab104274, 1:1000, ∼84 kDa), Mfn2 (CST, #9482, 1:1000, ∼86 kDa), Opa1 (CST, #80471, 1:1000, ∼100–120 kDa), Pink1 (CST, #6946, 1:1000, ∼63 kDa), cGAS (CST, #15102, 1:1000, ∼60 kDa), STING (CST, #13647, 1:1000, ∼42–45 kDa), TBK1 (CST, #3013, 1:1000, ∼84 kDa), p-TBK1 (CST, #5483, 1:1000, ∼84 kDa), COX IV (Abcam, ab14744, 1:2000, ∼17 kDa), β-actin (Proteintech, 66009-1-Ig, 1:5000, ∼43 kDa), and GAPDH (Proteintech, 60004-1-Ig, 1:5000, After washing, the membranes were incubated with HRP-conjugated secondary antibodies (goat anti-rabbit or goat anti-mouse IgG, CST, 1:5000) for 1 h at room temperature. .. The signals were visualized via an enhanced chemiluminescence (ECL) detection kit (Thermo Fisher Scientific) and imaged with the Bio-Rad ChemiDoc MP system.

    Blocking Assay:

    Article Title: STING activation promotes intestinal mucin secretion in IBD.
    Article Snippet: Background & aims: Goblet cells produce mucus protecting the intestinal epithelium.. Depleted goblet cells and a disrupted mucus layer are observed in inflammatory bowel diseases (IBD).. Remarkably, both deficiency and overactivation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway lead to goblet cell depletion in mice.

    FLAG-tag:

    Article Title: STING-ERO1 signaling exacerbates PARylation-mediated parthanatos in sepsis.
    Article Snippet: .. Antibodies used were as follows: STING (19851-1-AP, Proteintech), p-STING (72971, Cell Signaling Technology), p-TBK1 (5483, Cell Signaling Technology), TBK1 (38066, Cell Signaling Technology), pIRF3 (29047, Cell Signaling Technology), IRF3 (4302, Cell Signaling Technology), PARP1 (9532, Cell Signaling Technology), AIF (sc13116, Santa Cruz), pADPr (4335-MC-100, R&D Systems), Poly ADPribose (ALX-804-220-R100, ENZO Life Sciences), MIF (A11231, ABclonal), γH2AX (AP0687, ABclonal), β-actin (AC026, ABclonal), GAPDH (A19056, ABclonal), LC3 (A19665, ABclonal), Lamin B1 (AC057, ABclonal), ERO1 (67416-1-Ig, Proteintech), ERO1 (ab17716, Abcam), FLAG-tag (AE063, ABclonal; MA1-91878, Invitrogen), MycTag (AE010, ABclonal; AE070, ABclonal). ..



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    COPN mitigates retinal ischemia‒reperfusion injury by suppressing the <t>cGAS–STING–TBK1</t> signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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    Image Search Results


    COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Materials Today Bio

    Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

    doi: 10.1016/j.mtbio.2026.102974

    Figure Lengend Snippet: COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: The following primary antibodies were used: Drp1 (CST, #8570, 1:1000, ∼80 kDa), Fis1 (Proteintech, 10956-1-AP, 1:1000, ∼17 kDa), Mfn1 (Abcam, ab104274, 1:1000, ∼84 kDa), Mfn2 (CST, #9482, 1:1000, ∼86 kDa), Opa1 (CST, #80471, 1:1000, ∼100–120 kDa), Pink1 (CST, #6946, 1:1000, ∼63 kDa), cGAS (CST, #15102, 1:1000, ∼60 kDa), STING (CST, #13647, 1:1000, ∼42–45 kDa), TBK1 (CST, #3013, 1:1000, ∼84 kDa), p-TBK1 (CST, #5483, 1:1000, ∼84 kDa), COX IV (Abcam, ab14744, 1:2000, ∼17 kDa), β-actin (Proteintech, 66009-1-Ig, 1:5000, ∼43 kDa), and GAPDH (Proteintech, 60004-1-Ig, 1:5000, After washing, the membranes were incubated with HRP-conjugated secondary antibodies (goat anti-rabbit or goat anti-mouse IgG, CST, 1:5000) for 1 h at room temperature.

    Techniques: Quantitative Proteomics, Control, Activation Assay, Phospho-proteomics, Disruption, Western Blot