Review

anti phosphorylated irf3 (Cell Signaling Technology Inc)

Cell Signaling Technology Inc is a verified supplier

Cell Signaling Technology Inc manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Signaling Technology Inc anti phosphorylated irf3

A Heatmap showing the decreased expression of majority of ISGs compared SP to Control group (each group, n = 4) in HCT116 cells; SP treated 4 h. B qPCR testing the expression of CXCL10, ISG15, IFNB1, and IFIT1 in HCT116 cells. PAM3, LPS, and cGAMP treat HCT116 for 3 h. PAM3, Pam3CSK4, stimulates TLR2 ligand; LPS, stimulates TLR4 ligand; poly (I:C), stimulates MAVS; cGAMP, 2′3′-cGAMP, stimulates STING. Data are mean ± SEM from n = 4. C WB analysis in HCT116 pretreated with SP for 48 h, followed by a 3 h stimulation with cGAMP (left) and poly (I:C) (right); <t>p-IRF3,</t> IRF3 phosphorylate; p-TBK1, TBK1 phosphorylate; t-IRF3, total IRF3; t-TBK1, total TBK1. D ELISA analysis IFNβ secretion in HCT116 treated with cGAMP for 3 h after with or without infected SP for 48 h. Data are mean ± SEM from n = 3. E WB analysis STING protein in different cell lines treated with SP for 48 h in different MOI. F IF shows SP-GFP within HCT116 cells. ER, light blue; SP-GFP, green; Nucleus, DAPI, red. Scale bar = 15 μm, 5 μm. G ELISA analysis of IFNβ secretion in STING-KO HCT116. Data are mean ± SEM from n = 3. H Flow cytometry analysis of MHC-II⁺ macrophage populations following coculture with wild-type or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. I Flow cytometry analysis of CD206⁺ macrophage populations following coculture with WT or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. J Tumor volume (left) and tumor weight (right) in C57 mouse. STING-KO, knock out the gene of STING in MC38 cells. WT wild type; Data are mean ± SEM from n = 5. P values were determined by unpaired two-tailed t -tests unless otherwise specified (one-way ANOVA was used to multiple group comparisons). * p < 0.05, ** p < 0.01, *** p < 0.001. Source data are provided as a file.

Anti Phosphorylated Irf3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1419 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/phosphorylated+irf3+ser396/Phospho-IRF-3+(Ser396)+Rabbit+mAb/pmc12946332-455-21-25
Average 96 stars, based on 1419 article reviews

anti phosphorylated irf3 - by Bioz Stars, 2026-09

96/100 stars

Images

1) Product Images from "Stenotrophomonas promotes gastrointestinal tumor progression via STING degradation in tumour cells and mitigated immune response"

Article Title: Stenotrophomonas promotes gastrointestinal tumor progression via STING degradation in tumour cells and mitigated immune response

Journal: Nature Communications

doi: 10.1038/s41467-026-68649-0

Figure Legend Snippet: A Heatmap showing the decreased expression of majority of ISGs compared SP to Control group (each group, n = 4) in HCT116 cells; SP treated 4 h. B qPCR testing the expression of CXCL10, ISG15, IFNB1, and IFIT1 in HCT116 cells. PAM3, LPS, and cGAMP treat HCT116 for 3 h. PAM3, Pam3CSK4, stimulates TLR2 ligand; LPS, stimulates TLR4 ligand; poly (I:C), stimulates MAVS; cGAMP, 2′3′-cGAMP, stimulates STING. Data are mean ± SEM from n = 4. C WB analysis in HCT116 pretreated with SP for 48 h, followed by a 3 h stimulation with cGAMP (left) and poly (I:C) (right); p-IRF3, IRF3 phosphorylate; p-TBK1, TBK1 phosphorylate; t-IRF3, total IRF3; t-TBK1, total TBK1. D ELISA analysis IFNβ secretion in HCT116 treated with cGAMP for 3 h after with or without infected SP for 48 h. Data are mean ± SEM from n = 3. E WB analysis STING protein in different cell lines treated with SP for 48 h in different MOI. F IF shows SP-GFP within HCT116 cells. ER, light blue; SP-GFP, green; Nucleus, DAPI, red. Scale bar = 15 μm, 5 μm. G ELISA analysis of IFNβ secretion in STING-KO HCT116. Data are mean ± SEM from n = 3. H Flow cytometry analysis of MHC-II⁺ macrophage populations following coculture with wild-type or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. I Flow cytometry analysis of CD206⁺ macrophage populations following coculture with WT or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. J Tumor volume (left) and tumor weight (right) in C57 mouse. STING-KO, knock out the gene of STING in MC38 cells. WT wild type; Data are mean ± SEM from n = 5. P values were determined by unpaired two-tailed t -tests unless otherwise specified (one-way ANOVA was used to multiple group comparisons). * p < 0.05, ** p < 0.01, *** p < 0.001. Source data are provided as a file.

Techniques Used: Expressing, Control, Enzyme-linked Immunosorbent Assay, Infection, Flow Cytometry, Knock-Out, Two Tailed Test

Incubation:

Article Title: Identification of α-Mangostin as an Agonist of Human STING.
Article Snippet: A xanthone derivate DMXAA is a potent agonist of mouse STING (stimulator of interferon genes) but cannot activates human STING.. We here report that -Mangostin with the xanthone skeleton is an agonist of human STING but activates mouse STING to a lesser extent.. Protein and cellular assays indicate that -Mangostin binds to and activates human STING leading to activation of the downstream interferon regulatory factor (IRF) pathway, and production of type I interferons.

Article Title: The discovery of potent small molecule activators of human STING
Article Snippet: The adaptor protein STING plays a major role in innate immune sensing of cytosolic nucleic acids, by triggering a robust interferon response.. Despite the importance of this protein as a potential therapeutic target for serious unmet medical conditions including cancer and infectious disease there remains a paucity of STING ligands.. Starting with a benzothiazinone series of Jo urn al Pr e-p roo f

Article Title: Development of Small-Molecule STING Activators for Cancer Immunotherapy
Article Snippet: The membrane was blocked with 5% BSA in Tris-buffered saline with Tween-20 (TBST; BIOSESANG) solution for 1 h at room temperature, followed by washing with TBST. .. Membranes were incubated with the following antibodies: (1) at 1:1000 dilution—phosphorylated STAT1(Tyr701) (#7649; Cell Signaling, Danvers, MA, USA), phosphorylated TBK1 (Ser172) (#5483; Cell Signaling), phosphorylated IRF3 (Ser396) (#4947S; Cell Signaling), phosphorylated STING (S366) (#19781; Cell Signaling), STAT1 (#9172; Cell Signaling), IRF3 (#11904; Cell Signaling), TBK1 (#3504; Cell Signaling), STING (#13647; Cell Signaling), and (2) at 1:3000 dilution—β-actin (#4970; Cell Signaling). .. HRP-conjugated secondary antibody (#7074; Cell Signaling) was used at a dilution of 1:3000.

Article Title: G10 is a direct activator of human STING
Article Snippet: 10 μg of extracted protein was electrophoresed in 10% SDS-PAGE gels and transferred onto Immobilon-P membranes (Millipore). .. Blots were incubated with antibodies specific for phosphorylated STING (Ser366), phosphorylated IRF3 (Ser396), total STING, Actin (Cell Signaling) and IRF3 (Abcam) as shown in . .. Anti-rabbit HRP label secondary antibody (Abcam) and Clarity Max TM western ECL substrate (Biorad—cat# 1705062) were used for visualization of bands using a BioRad XRS plus imager.

other:

Article Title: Polycomb chromobox Cbx2 enhances antiviral innate immunity by promoting Jmjd3-mediated demethylation of H3K27 at the Ifnb promoter
Article Snippet: Antibodies against Myc-tag (2272, 2276, 2040), Flag-tag (14793), phosphorylated IRF3 (Ser396) (#4947), phosphorylated NF-κB p65 (Ser536) (#3033), and Normal Rabbit IgG (#2729) were from Cell Signaling Technology.

Image Search Results

Journal: Nature Communications

Article Title: Stenotrophomonas promotes gastrointestinal tumor progression via STING degradation in tumour cells and mitigated immune response

doi: 10.1038/s41467-026-68649-0

Figure Lengend Snippet: A Heatmap showing the decreased expression of majority of ISGs compared SP to Control group (each group, n = 4) in HCT116 cells; SP treated 4 h. B qPCR testing the expression of CXCL10, ISG15, IFNB1, and IFIT1 in HCT116 cells. PAM3, LPS, and cGAMP treat HCT116 for 3 h. PAM3, Pam3CSK4, stimulates TLR2 ligand; LPS, stimulates TLR4 ligand; poly (I:C), stimulates MAVS; cGAMP, 2′3′-cGAMP, stimulates STING. Data are mean ± SEM from n = 4. C WB analysis in HCT116 pretreated with SP for 48 h, followed by a 3 h stimulation with cGAMP (left) and poly (I:C) (right); p-IRF3, IRF3 phosphorylate; p-TBK1, TBK1 phosphorylate; t-IRF3, total IRF3; t-TBK1, total TBK1. D ELISA analysis IFNβ secretion in HCT116 treated with cGAMP for 3 h after with or without infected SP for 48 h. Data are mean ± SEM from n = 3. E WB analysis STING protein in different cell lines treated with SP for 48 h in different MOI. F IF shows SP-GFP within HCT116 cells. ER, light blue; SP-GFP, green; Nucleus, DAPI, red. Scale bar = 15 μm, 5 μm. G ELISA analysis of IFNβ secretion in STING-KO HCT116. Data are mean ± SEM from n = 3. H Flow cytometry analysis of MHC-II⁺ macrophage populations following coculture with wild-type or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. I Flow cytometry analysis of CD206⁺ macrophage populations following coculture with WT or STING-KO HCT116 cells. Data are mean ± SEM from n = 3. J Tumor volume (left) and tumor weight (right) in C57 mouse. STING-KO, knock out the gene of STING in MC38 cells. WT wild type; Data are mean ± SEM from n = 5. P values were determined by unpaired two-tailed t -tests unless otherwise specified (one-way ANOVA was used to multiple group comparisons). * p < 0.05, ** p < 0.01, *** p < 0.001. Source data are provided as a file.

Article Snippet: The primary antibodies included anti-β-tubulin (cat: ARG62347 , Arigo), anti-GAPDH (cat: 2118, Cell Signaling Technology), anti-IRF3 (cat: 4302, Cell Signaling Technology), anti-phosphorylated IRF3 (cat: 4947, Cell Signaling Technology), anti-TBK1 (cat: 3504S, Cell Signaling Technology), anti-phosphorylated TBK1 (cat: 5483S, Cell Signaling Technology), anti-STING (cat: 13647, Cell Signaling Technology) and anti-phosphorylated STING (cat: 50907S, Cell Signaling Technology), anti-SEL1L (cat: 29801-1-AP, Proteintech), anti-Phospho-PERK (cat: 3179 T, Cell Signaling Technology), anti-PERK (cat: 3192 T, Cell Signaling Technology), anti-cGAS (cat:79978, Cell Signaling Technology), anti-IRE1α (cat: 3294, Cell Signaling Technology), anti-ATF-6 (cat: 65880, Cell Signaling Technology), anti-XBP-1s(cat: 40435, Cell Signaling Technology).

Techniques: Expressing, Control, Enzyme-linked Immunosorbent Assay, Infection, Flow Cytometry, Knock-Out, Two Tailed Test

The inhibitory activity of HCQ-L and HCQ-L-P12 on NF-kB activation, pro-inflammatory cytokine production, and endosomal/lysosomal acidification. ( a ) The representative immunoblots showing the effects of HCQ-L and HCQ-L-P12 on the phosphorylation of p65 (p-p65) and IRF3 (p-IRF3) as well as the degradation of IκBα in the THP-1 cell-derived macrophages upon LPS stimulation over time (0–60 min); β-actin as the internal control. ( b – d ) The densitometry analysis of p-p65 ( b ), IκBα ( c ), and p-IRF3 ( d ) from the immunoblots in ( a ); N = 3; ns: not significant, #, * p < 0.05, ## p < 0.01 vs. LPS group. ( e – g ) The effects of HCQ-L and HCQ-L-P12 on the LPS-induced production of the pro-inflammatory cytokines IL-6 ( e ), TNF-α ( f ), and MCP-1 ( g ) in THP-1 cell-derived macrophages; N = 4 (for IL-6), 5 (for TNF-α), and 3 (for MCP-1); ns: not significant, * p < 0.05, **** p < 0.0001 vs. LPS group unless otherwise specified. ( h ) The representative confocal images showing the effects of HCQ-L and HCQ-L-P12 on the endosomal acidification probed by pHrodo red (red) (10 μg/mL) and fluorescein (green) (20 μg/mL) labeled dextran in THP-1 cell-derived macrophages overnight; chloroquine (CQ, 30 μM) was used as the positive control; scale bar = 5 μm. ( i ) The ratio of fluorescein/pHrodo red fluorescence intensities quantified from ( i ); N ≥ 40 cells from 2 independent experiments; ns: not significant, *** p < 0.001, **** p < 0.0001 vs. untreated control unless otherwise specified. LPS = 10 ng/mL, HCQ-L/HCQ-L-P12 = 50 μM (HCQ concentration).

Journal: Journal of Functional Biomaterials

Article Title: Hexapeptide-Liposome Nanosystem for the Delivery of Endosomal pH Modulator to Treat Acute Lung Injury

doi: 10.3390/jfb16120450

Figure Lengend Snippet: The inhibitory activity of HCQ-L and HCQ-L-P12 on NF-kB activation, pro-inflammatory cytokine production, and endosomal/lysosomal acidification. ( a ) The representative immunoblots showing the effects of HCQ-L and HCQ-L-P12 on the phosphorylation of p65 (p-p65) and IRF3 (p-IRF3) as well as the degradation of IκBα in the THP-1 cell-derived macrophages upon LPS stimulation over time (0–60 min); β-actin as the internal control. ( b – d ) The densitometry analysis of p-p65 ( b ), IκBα ( c ), and p-IRF3 ( d ) from the immunoblots in ( a ); N = 3; ns: not significant, #, * p < 0.05, ## p < 0.01 vs. LPS group. ( e – g ) The effects of HCQ-L and HCQ-L-P12 on the LPS-induced production of the pro-inflammatory cytokines IL-6 ( e ), TNF-α ( f ), and MCP-1 ( g ) in THP-1 cell-derived macrophages; N = 4 (for IL-6), 5 (for TNF-α), and 3 (for MCP-1); ns: not significant, * p < 0.05, **** p < 0.0001 vs. LPS group unless otherwise specified. ( h ) The representative confocal images showing the effects of HCQ-L and HCQ-L-P12 on the endosomal acidification probed by pHrodo red (red) (10 μg/mL) and fluorescein (green) (20 μg/mL) labeled dextran in THP-1 cell-derived macrophages overnight; chloroquine (CQ, 30 μM) was used as the positive control; scale bar = 5 μm. ( i ) The ratio of fluorescein/pHrodo red fluorescence intensities quantified from ( i ); N ≥ 40 cells from 2 independent experiments; ns: not significant, *** p < 0.001, **** p < 0.0001 vs. untreated control unless otherwise specified. LPS = 10 ng/mL, HCQ-L/HCQ-L-P12 = 50 μM (HCQ concentration).

Article Snippet: The primary antibodies against IκBα (9242S), phosphorylated p65 (p-p65, 3033S), β-actin (8457S), and phosphorylated IRF3 (p-IRF3, 4947S), as well as the HRP-linked anti-rabbit antibody (7074S), were all acquired from Cell Signaling Technology (Boston, MA, USA).

Techniques: Activity Assay, Activation Assay, Western Blot, Phospho-proteomics, Derivative Assay, Control, Labeling, Positive Control, Fluorescence, Concentration Assay