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p irf3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p irf3
    Schematic illustration of the ROS-responsive on-demand mild photothermal cascade platform for tendon rejuvenation in Achilles tendinopathy. The platform strategically modulates the <t>mitochondrial-cGAS-STING-IRF3/NF-κB</t> signaling axis and induces heat shock protein 70 (HSP70) expression to attenuate oxidative stress and cellular senescence within tendon stem/progenitor cells (TSPCs). Consequently, it promotes tenogenic differentiation while abrogating aberrant osteogenic/chondrogenic lineage commitment. This cascade effect ultimately mitigates heterotopic ossification, enhances structural tendon regeneration, restores biomechanical function, and alleviates pain. Nanoparticle nomenclature: LA-NPs and TPA-TCNQ-NPs denote nanoparticles encapsulating LA or TPA-TCNQ individually; LT-NPs refers to the composite formulation consisting of a mixture of LA-NPs and TPA-TCNQ-NPs; and LT-NPs-NIR represents the LT-NPs mixture following 808 nm near-infrared (NIR) irradiation to activate the photothermal response and controlled payload release.
    P Irf3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 632 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+irf3+ser396/Phospho-IRF-3+(Ser396)+Rabbit+mAb/pmc12813888-103-34-36
    Average 96 stars, based on 632 article reviews
    p irf3 - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation"

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.01.004

    Schematic illustration of the ROS-responsive on-demand mild photothermal cascade platform for tendon rejuvenation in Achilles tendinopathy. The platform strategically modulates the mitochondrial-cGAS-STING-IRF3/NF-κB signaling axis and induces heat shock protein 70 (HSP70) expression to attenuate oxidative stress and cellular senescence within tendon stem/progenitor cells (TSPCs). Consequently, it promotes tenogenic differentiation while abrogating aberrant osteogenic/chondrogenic lineage commitment. This cascade effect ultimately mitigates heterotopic ossification, enhances structural tendon regeneration, restores biomechanical function, and alleviates pain. Nanoparticle nomenclature: LA-NPs and TPA-TCNQ-NPs denote nanoparticles encapsulating LA or TPA-TCNQ individually; LT-NPs refers to the composite formulation consisting of a mixture of LA-NPs and TPA-TCNQ-NPs; and LT-NPs-NIR represents the LT-NPs mixture following 808 nm near-infrared (NIR) irradiation to activate the photothermal response and controlled payload release.
    Figure Legend Snippet: Schematic illustration of the ROS-responsive on-demand mild photothermal cascade platform for tendon rejuvenation in Achilles tendinopathy. The platform strategically modulates the mitochondrial-cGAS-STING-IRF3/NF-κB signaling axis and induces heat shock protein 70 (HSP70) expression to attenuate oxidative stress and cellular senescence within tendon stem/progenitor cells (TSPCs). Consequently, it promotes tenogenic differentiation while abrogating aberrant osteogenic/chondrogenic lineage commitment. This cascade effect ultimately mitigates heterotopic ossification, enhances structural tendon regeneration, restores biomechanical function, and alleviates pain. Nanoparticle nomenclature: LA-NPs and TPA-TCNQ-NPs denote nanoparticles encapsulating LA or TPA-TCNQ individually; LT-NPs refers to the composite formulation consisting of a mixture of LA-NPs and TPA-TCNQ-NPs; and LT-NPs-NIR represents the LT-NPs mixture following 808 nm near-infrared (NIR) irradiation to activate the photothermal response and controlled payload release.

    Techniques Used: Expressing, Formulation, Irradiation

    LT-NPs-NIR regulate the mtDNA-STING-IRF3/NF-κB pathway in macrophages. (A) Principal component analysis (PCA) of transcriptomic data from RAW 264.7 cells under different treatments. (B) Volcano plots comparing H 2 O 2 vs. Control (left) and LT-NPs-NIR vs. H 2 O 2 (right). (C) Heatmap of differentially expressed genes (DEGs) with hierarchical clustering. (D, E) Gene Ontology (GO), KEGG, and Gene Set Enrichment Analysis (GSEA) for H 2 O 2 vs. Control (D) and LT-NPs-NIR vs. H 2 O 2 (E). (F) Multi-SIM imaging showing mtDNA (magenta) and the mitochondrial outer membrane protein TOMM20 (green), with quantification of their colocalization. (G) Western blot analysis of key proteins in the cGAS-STING-NF-κB axis. Scale bar: 5 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
    Figure Legend Snippet: LT-NPs-NIR regulate the mtDNA-STING-IRF3/NF-κB pathway in macrophages. (A) Principal component analysis (PCA) of transcriptomic data from RAW 264.7 cells under different treatments. (B) Volcano plots comparing H 2 O 2 vs. Control (left) and LT-NPs-NIR vs. H 2 O 2 (right). (C) Heatmap of differentially expressed genes (DEGs) with hierarchical clustering. (D, E) Gene Ontology (GO), KEGG, and Gene Set Enrichment Analysis (GSEA) for H 2 O 2 vs. Control (D) and LT-NPs-NIR vs. H 2 O 2 (E). (F) Multi-SIM imaging showing mtDNA (magenta) and the mitochondrial outer membrane protein TOMM20 (green), with quantification of their colocalization. (G) Western blot analysis of key proteins in the cGAS-STING-NF-κB axis. Scale bar: 5 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Techniques Used: Control, Imaging, Membrane, Western Blot

    LT-NPs-NIR attenuate oxidative stress, preserve mitochondrial integrity, and suppress senescence in TSPCs by inhibiting the mtDNA-STING-NF-κB axis. (A) Schematic of the experimental design. (B) TSPC proliferation assessed by CCK-8 assay. (C, E) Immunofluorescence staining and quantification of HSP70 (n = 3). (D, F) Mitochondrial membrane potential (ΔΨm) visualized by JC-1 staining (red: high potential; green: low potential) and quantification. (G) Multi-SIM of mtDNA (magenta) and TOMM20 (green) with colocalization analysis. (H) Western blot of cGAS-STING-IRF3-NF-κB pathway proteins. (I, K) Colony-forming unit fibroblast (CFU-F) assay and quantification of self-renewal capacity (n = 3). (J) Senescence-associated β-galactosidase (SA-β-gal) activity. (L, M) Apoptosis analysis by Annexin V/PI flow cytometry and quantification (n = 3). Scale bars: 100 μm (C); 5 μm (D, G); 200 μm (J). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
    Figure Legend Snippet: LT-NPs-NIR attenuate oxidative stress, preserve mitochondrial integrity, and suppress senescence in TSPCs by inhibiting the mtDNA-STING-NF-κB axis. (A) Schematic of the experimental design. (B) TSPC proliferation assessed by CCK-8 assay. (C, E) Immunofluorescence staining and quantification of HSP70 (n = 3). (D, F) Mitochondrial membrane potential (ΔΨm) visualized by JC-1 staining (red: high potential; green: low potential) and quantification. (G) Multi-SIM of mtDNA (magenta) and TOMM20 (green) with colocalization analysis. (H) Western blot of cGAS-STING-IRF3-NF-κB pathway proteins. (I, K) Colony-forming unit fibroblast (CFU-F) assay and quantification of self-renewal capacity (n = 3). (J) Senescence-associated β-galactosidase (SA-β-gal) activity. (L, M) Apoptosis analysis by Annexin V/PI flow cytometry and quantification (n = 3). Scale bars: 100 μm (C); 5 μm (D, G); 200 μm (J). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Techniques Used: CCK-8 Assay, Immunofluorescence, Staining, Membrane, Western Blot, Activity Assay, Flow Cytometry

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    Ubiquitin Proteomics:

    Article Title: Ubiquitination by HRD1 is essential for TLR3 trafficking and its innate immune signaling.
    Article Snippet: For Endo H treatment, the lysates were treated with Endo H or PNGase F (New England BioLab) per manufacturer’s instruction. .. Antibodies used in this study were: Flag (Sigma F1804; 1:2000); HA AR TI CL E IN P RE SS (Proteintech 51064-2-AP; 1:4000), HRD1 (Proteintech 13473-1-AP; 1:1000), SEL1L (Abclonal; A12073, 1:2000), IRE1α (Cell Signaling 3294; 1:3000), PERK (Proteintech 20582-1-AP; 1:3000), Eif2α(Cell Signaling 5324; 1:3000), p-Eif2α(Cell Signaling 5324; 1:2000), β-tubulin (Proteintech 10068-1-AP; 1:3000), HSP90 (Proteintech 13171-1-AP; 1:5000), Myc (ABclonal AE010; 1:2000), V5 (ABclonal AE017; 1:2000), phospho-IκBα (ABclonal AP0707; 1:1000), HRS (ABclonal A1790; 1:3000), TSG101 (ABclonal A1692; 1:1000), VPS36 (ABclonal A15157; 1:1000), TLR3 (NOVUS NBP2-24875; 2 μg/ml), , p-TBK1 (Ser172) (Cell Signaling D52C2; 1:1000), TBK1 (Cell Signaling E9H5S; 1:2000), p-IRF3 (Ser396) (Cell Signaling D601M; 1:2000), IRF3 (Cell Signaling D83B9; 1:2000), IκBα (Cell Signaling 9242; 1:2000), β-actin (Cell Signaling 13E5; 1:5000), p65 (Cell Signaling D14E12; 1:2000), phospho-p65 (Cell Signaling 93H1; 1:1000), Ubiquitin (linkagespecific K48) (Cell Signaling D9D5; 1:2000), Ubiquitin (linkage-specific K63) (Cell Signaling D7A11; 1:2000), GOLPH2 (ABclonal A26409PM; 1:1000), EEA1 (ABclonal A5057; 1:2000), Ubiquitin (Santa Cruz P4D1; 1:200), TGN38 (Santa Cruz sc-166594; 1:200), and mouse IgG (Santa Cruz sc-2025), Rabbit IgG (Abclonal; AC005)ERK1/2 (Cell Signaling 4695; 1:2000), pERK1/2 (Cell Signaling 9101; 1:2000), STAT1 (Cell Signaling 14994; 1:2000), p-STAT1 (Cell Signaling 9167;1:2000). .. Western blot band density was quantitated by the use of Image Lab software 4.1 on the ChemiDOC XRS+ system (Bio-Rad).

    Staining:

    Article Title: IRG1/itaconate/NRF2/GSH axis in tumor-associated macrophages drives therapy resistance and immune evasion in BRCA1-deficient breast cancer
    Article Snippet: Viable cells were identified using the LIVE/DEAD Fixable Aqua Dead Cell Stain (L34965, Thermo Fisher Scientific) for 30 minutes on ice. .. Cells were subsequently stained with phospho-specific antibodies against p-TBK1 (Ser172) (1:50; 5483, Cell Signaling Technology) or p-IRF3 (Ser396) (1:50; 29047, Cell Signaling Technology) for 30 minutes on ice. ..



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    Schematic illustration of the ROS-responsive on-demand mild photothermal cascade platform for tendon rejuvenation in Achilles tendinopathy. The platform strategically modulates the mitochondrial-cGAS-STING-IRF3/NF-κB signaling axis and induces heat shock protein 70 (HSP70) expression to attenuate oxidative stress and cellular senescence within tendon stem/progenitor cells (TSPCs). Consequently, it promotes tenogenic differentiation while abrogating aberrant osteogenic/chondrogenic lineage commitment. This cascade effect ultimately mitigates heterotopic ossification, enhances structural tendon regeneration, restores biomechanical function, and alleviates pain. Nanoparticle nomenclature: LA-NPs and TPA-TCNQ-NPs denote nanoparticles encapsulating LA or TPA-TCNQ individually; LT-NPs refers to the composite formulation consisting of a mixture of LA-NPs and TPA-TCNQ-NPs; and LT-NPs-NIR represents the LT-NPs mixture following 808 nm near-infrared (NIR) irradiation to activate the photothermal response and controlled payload release.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: Schematic illustration of the ROS-responsive on-demand mild photothermal cascade platform for tendon rejuvenation in Achilles tendinopathy. The platform strategically modulates the mitochondrial-cGAS-STING-IRF3/NF-κB signaling axis and induces heat shock protein 70 (HSP70) expression to attenuate oxidative stress and cellular senescence within tendon stem/progenitor cells (TSPCs). Consequently, it promotes tenogenic differentiation while abrogating aberrant osteogenic/chondrogenic lineage commitment. This cascade effect ultimately mitigates heterotopic ossification, enhances structural tendon regeneration, restores biomechanical function, and alleviates pain. Nanoparticle nomenclature: LA-NPs and TPA-TCNQ-NPs denote nanoparticles encapsulating LA or TPA-TCNQ individually; LT-NPs refers to the composite formulation consisting of a mixture of LA-NPs and TPA-TCNQ-NPs; and LT-NPs-NIR represents the LT-NPs mixture following 808 nm near-infrared (NIR) irradiation to activate the photothermal response and controlled payload release.

    Article Snippet: After blocking for 1 h, membranes were incubated overnight at 4 °C with primary antibodies against STING (13647, CST, USA; A21051, Abclonal, China), p-STING (72971, CST, USA; AF7416, Affinity, China), IRF3 (ab68481, Abcam, UK), p-IRF3 (29047, CST, USA), P65 (A22331, Abclonal, China; 8242, CST, USA), p-P65 (AP0124, Abclonal, China), P53 (10442-1-AP, Proteintech, USA), SOX9 (sc-166505, Santa Cruz, USA), BMP-2 (ab284387, abcam, USA), OCN (sc-390877, Santa Cruz, USA), and iNOS (ab178945, Abcam, USA).

    Techniques: Expressing, Formulation, Irradiation

    LT-NPs-NIR regulate the mtDNA-STING-IRF3/NF-κB pathway in macrophages. (A) Principal component analysis (PCA) of transcriptomic data from RAW 264.7 cells under different treatments. (B) Volcano plots comparing H 2 O 2 vs. Control (left) and LT-NPs-NIR vs. H 2 O 2 (right). (C) Heatmap of differentially expressed genes (DEGs) with hierarchical clustering. (D, E) Gene Ontology (GO), KEGG, and Gene Set Enrichment Analysis (GSEA) for H 2 O 2 vs. Control (D) and LT-NPs-NIR vs. H 2 O 2 (E). (F) Multi-SIM imaging showing mtDNA (magenta) and the mitochondrial outer membrane protein TOMM20 (green), with quantification of their colocalization. (G) Western blot analysis of key proteins in the cGAS-STING-NF-κB axis. Scale bar: 5 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR regulate the mtDNA-STING-IRF3/NF-κB pathway in macrophages. (A) Principal component analysis (PCA) of transcriptomic data from RAW 264.7 cells under different treatments. (B) Volcano plots comparing H 2 O 2 vs. Control (left) and LT-NPs-NIR vs. H 2 O 2 (right). (C) Heatmap of differentially expressed genes (DEGs) with hierarchical clustering. (D, E) Gene Ontology (GO), KEGG, and Gene Set Enrichment Analysis (GSEA) for H 2 O 2 vs. Control (D) and LT-NPs-NIR vs. H 2 O 2 (E). (F) Multi-SIM imaging showing mtDNA (magenta) and the mitochondrial outer membrane protein TOMM20 (green), with quantification of their colocalization. (G) Western blot analysis of key proteins in the cGAS-STING-NF-κB axis. Scale bar: 5 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After blocking for 1 h, membranes were incubated overnight at 4 °C with primary antibodies against STING (13647, CST, USA; A21051, Abclonal, China), p-STING (72971, CST, USA; AF7416, Affinity, China), IRF3 (ab68481, Abcam, UK), p-IRF3 (29047, CST, USA), P65 (A22331, Abclonal, China; 8242, CST, USA), p-P65 (AP0124, Abclonal, China), P53 (10442-1-AP, Proteintech, USA), SOX9 (sc-166505, Santa Cruz, USA), BMP-2 (ab284387, abcam, USA), OCN (sc-390877, Santa Cruz, USA), and iNOS (ab178945, Abcam, USA).

    Techniques: Control, Imaging, Membrane, Western Blot

    LT-NPs-NIR attenuate oxidative stress, preserve mitochondrial integrity, and suppress senescence in TSPCs by inhibiting the mtDNA-STING-NF-κB axis. (A) Schematic of the experimental design. (B) TSPC proliferation assessed by CCK-8 assay. (C, E) Immunofluorescence staining and quantification of HSP70 (n = 3). (D, F) Mitochondrial membrane potential (ΔΨm) visualized by JC-1 staining (red: high potential; green: low potential) and quantification. (G) Multi-SIM of mtDNA (magenta) and TOMM20 (green) with colocalization analysis. (H) Western blot of cGAS-STING-IRF3-NF-κB pathway proteins. (I, K) Colony-forming unit fibroblast (CFU-F) assay and quantification of self-renewal capacity (n = 3). (J) Senescence-associated β-galactosidase (SA-β-gal) activity. (L, M) Apoptosis analysis by Annexin V/PI flow cytometry and quantification (n = 3). Scale bars: 100 μm (C); 5 μm (D, G); 200 μm (J). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR attenuate oxidative stress, preserve mitochondrial integrity, and suppress senescence in TSPCs by inhibiting the mtDNA-STING-NF-κB axis. (A) Schematic of the experimental design. (B) TSPC proliferation assessed by CCK-8 assay. (C, E) Immunofluorescence staining and quantification of HSP70 (n = 3). (D, F) Mitochondrial membrane potential (ΔΨm) visualized by JC-1 staining (red: high potential; green: low potential) and quantification. (G) Multi-SIM of mtDNA (magenta) and TOMM20 (green) with colocalization analysis. (H) Western blot of cGAS-STING-IRF3-NF-κB pathway proteins. (I, K) Colony-forming unit fibroblast (CFU-F) assay and quantification of self-renewal capacity (n = 3). (J) Senescence-associated β-galactosidase (SA-β-gal) activity. (L, M) Apoptosis analysis by Annexin V/PI flow cytometry and quantification (n = 3). Scale bars: 100 μm (C); 5 μm (D, G); 200 μm (J). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After blocking for 1 h, membranes were incubated overnight at 4 °C with primary antibodies against STING (13647, CST, USA; A21051, Abclonal, China), p-STING (72971, CST, USA; AF7416, Affinity, China), IRF3 (ab68481, Abcam, UK), p-IRF3 (29047, CST, USA), P65 (A22331, Abclonal, China; 8242, CST, USA), p-P65 (AP0124, Abclonal, China), P53 (10442-1-AP, Proteintech, USA), SOX9 (sc-166505, Santa Cruz, USA), BMP-2 (ab284387, abcam, USA), OCN (sc-390877, Santa Cruz, USA), and iNOS (ab178945, Abcam, USA).

    Techniques: CCK-8 Assay, Immunofluorescence, Staining, Membrane, Western Blot, Activity Assay, Flow Cytometry