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Cell Signaling Technology Inc p irf3
P Irf3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+irf3/pmc12989726-434-17-26
Average 86 stars, based on 1 article reviews

p irf3 - by Bioz Stars, 2026-10

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Blocking Assay:

Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation
Article Snippet: Equal amounts of protein were separated by SDS-PAGE and transferred onto PVDF membranes (Millipore, USA). .. 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). ..

Incubation:

Article Title: Short-chain acyl-CoA dehydrogenase initiates mtDNA demethylation and leakage to fuel antitumor immunity in colorectal cancer.
Article Snippet: .. The membranes were washed with TBST and incubated overnight at 4 °C with primary antibodies, including ACADS (#AP75024, Abcepta, Jiangsu, China), DNMT1 (#NB10056519AF594, NOVUS), cGAS (Cat#31659, Cell Signaling Technology), p-STING (#PA5-105674, Invitrogen), STING (#A3575, ABclonal), p-TBK1 (#AP1026, ABclonal), TBK1 (#AF8103, Beyotime), p-IRF3 (#4947, Cell Signaling Technology), IRF3 (#4302, Cell Signaling Technology), BAX (#A0207, ABclonal), VDAC1 (#A19707, ABclonal), VDAC3 (#55260-1-AP, Proteintech), HSP60 (#AF0186, Beyotime), PHB1 (#10787-1-AP, Proteintech), Lamin B1 (#ab16048, Abcam), HA (#51064-2-AP, Proteintech), TFAM (#A13552, ABclonal), NRF1 (#12482-1-AP, Proteintech), PGC1α (#66369-1-Ig, Proteintech), Twinkle (#18793-1-AP, Proteintech), POLG (#AP14948B, Abcepta), and β-actin (#66009-1-Ig, Proteintech). .. Following incubation with primary antibody, the membranes were washed 3 times with TBST and then hybridized with the corresponding secondary antibody at room temperature for 2 h. In certain instances, the membrane was subjected to washing with primary and secondary antibody removal solution (#P0025, Beyotime), followed by reincubation with either the indicated antibody or a loading control β-actin antibody, along with the corresponding secondary antibodies.

Article Title: Dual-engineering metalloimmunotherapy mediates Staphylococcus aureus virulence silencing and biofilm immune microenvironment reprogramming against implant-associated infections
Article Snippet: .. Primary antibodies specific to the target proteins were incubated with the membranes overnight at 4 °C, including P-IRF3, IRF3, P-TBK1, TBK1, P-STING, STING, P-p65 and p65 (CST, USA). ..

Article Title: Short-chain acyl-CoA dehydrogenase initiates mtDNA demethylation and leakage to fuel antitumor immunity in colorectal cancer
Article Snippet: .. The membranes were washed with TBST and incubated overnight at 4 °C with primary antibodies, including ACADS (#AP75024, Abcepta, Jiangsu, China), DNMT1 (#NB100-56519AF594, NOVUS), cGAS (Cat#31659, Cell Signaling Technology), p-STING (#PA5-105674, Invitrogen), STING (#A3575, ABclonal), p-TBK1 (#AP1026, ABclonal), TBK1 (#AF8103, Beyotime), p-IRF3 (#4947, Cell Signaling Technology), IRF3 (#4302, Cell Signaling Technology), BAX (#A0207, ABclonal), VDAC1 (#A19707, ABclonal), VDAC3 (#55260-1-AP, Proteintech), HSP60 (#AF0186, Beyotime), PHB1 (#10787-1-AP, Proteintech), Lamin B1 (#ab16048, Abcam), HA (#51064-2-AP, Proteintech), TFAM (#A13552, ABclonal), NRF1 (#12482-1-AP, Proteintech), PGC1α (#66369-1-Ig, Proteintech), Twinkle (#18793-1-AP, Proteintech), POLG (#AP14948B, Abcepta), and β-actin (#66009-1-Ig, Proteintech). .. Following incubation with primary antibody, the membranes were washed 3 times with TBST and then hybridized with the corresponding secondary antibody at room temperature for 2 h. In certain instances, the membrane was subjected to washing with primary and secondary antibody removal solution (#P0025, Beyotime), followed by reincubation with either the indicated antibody or a loading control β-actin antibody, along with the corresponding secondary antibodies.

Multiple Displacement Amplification:

Article Title: Triphenylphosphine bromide enhances the effect of nano-micellar drug delivery system loaded with ROS inhibitor TEMPO on acute lung injury.
Article Snippet: The JEM-2100 Plus transmission electron microscope (TEM) was purchased from Japan Electronics Corporation; The Zetasizer Nano ZSE nanoparticle potential analyzer was purchased from Malvern Instruments Limited in the UK; The Cell Insight CX7 LZR laser confocal high content screening (HCS) AR TIC LE IN PR ES S platform was purchased from Thermo Fisher Scientific (China) Co., Ltd; CytoFLEX flow cytometer was purchased from Beckman Corporation in the United States; TGL-16M desktop high-speed freeze centrifuge purchased from Jinan Cunchang Biotechnology Co., Ltd. Cytokine interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor (TNF-α) kits were obtained eBioscience. .. Superoxide Dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), oxidized glutathione (GSSG) were purchased from Nanjing Jiancheng Biotechnology Co., Ltd. cGAS (#79978), STING (#13647), p-IRF3 (#79945), IRF3 (#4302), p-NF-κBp65 (#3033), NF-κBp65 (#8242) and GAPDH (#5174) antibodies were purchased from Cell Signaling Technology Company. ..

Image Search Results

Decreased lactylation of pyruvate dehydrogenase E1 component subunit alpha (PDHA1) at Lys336 facilitates its dephosphorylation and drives a metabolic shift. (A) Pulmonary vascular endothelial cells (PVECs) were treated with D-galactose (D-gal; 30 mg/ml) for 24 h. Cell lysates were immunoprecipitated with PDHA1 antibody-conjugated Protein A/G Agarose, followed by Western blot for the lactylation of PDHA1 using anti-pan-lactyl antibodies. (B) PDHA1-K336R mutation increased pyruvate dehydrogenase complex (PDHC) activity in mouse primary PVECs. (C) Primary murine PVECs were cotransfected with wild-type PDHA1 WT or PDHA1-K336R mutant. Cell lysates were immunoprecipitated with PDHA1 antibody-conjugated Protein A/G Agarose, followed by a Western blot for the phosphorylation of PDHA1 using pan p-serine antibodies. (D and E) Lactyl-lysine protein level and the phosphorylation level at PDHA1 S293 were determined. (F and G) Quantification of intracellular and extracellular lactate levels. (H and I) The oxygen consumption rate (OCR) of PVECs transfected with the PDHA1-K336R mutant was measured using Seahorse XF24 Analyzer. (J and K) Statistical analyses of adenosine triphosphate (ATP)-linked respiration and maximal respiration. (L and M) The expression of oxidative phosphorylation (OXPHOS)-related proteins in PVECs transfected with the PDHA1-K336R mutant was detected by Western blot analysis. (N) Senescence-associated β-galactosidase (SA-β-gal) staining was assessed in mouse primary PVECs with PDHA1 WT or PDHA1 K336R (scale bar = 20 μm). (O and P) p53, p21, p16, and phosphorylated histone H2AX (γ-H2AX) protein levels in PVECs with PDHA1 WT or PDHA1 K336R were detected by Western blot. n = 3. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Journal: Research

Article Title: PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence

doi: 10.34133/research.1398

Figure Lengend Snippet: Decreased lactylation of pyruvate dehydrogenase E1 component subunit alpha (PDHA1) at Lys336 facilitates its dephosphorylation and drives a metabolic shift. (A) Pulmonary vascular endothelial cells (PVECs) were treated with D-galactose (D-gal; 30 mg/ml) for 24 h. Cell lysates were immunoprecipitated with PDHA1 antibody-conjugated Protein A/G Agarose, followed by Western blot for the lactylation of PDHA1 using anti-pan-lactyl antibodies. (B) PDHA1-K336R mutation increased pyruvate dehydrogenase complex (PDHC) activity in mouse primary PVECs. (C) Primary murine PVECs were cotransfected with wild-type PDHA1 WT or PDHA1-K336R mutant. Cell lysates were immunoprecipitated with PDHA1 antibody-conjugated Protein A/G Agarose, followed by a Western blot for the phosphorylation of PDHA1 using pan p-serine antibodies. (D and E) Lactyl-lysine protein level and the phosphorylation level at PDHA1 S293 were determined. (F and G) Quantification of intracellular and extracellular lactate levels. (H and I) The oxygen consumption rate (OCR) of PVECs transfected with the PDHA1-K336R mutant was measured using Seahorse XF24 Analyzer. (J and K) Statistical analyses of adenosine triphosphate (ATP)-linked respiration and maximal respiration. (L and M) The expression of oxidative phosphorylation (OXPHOS)-related proteins in PVECs transfected with the PDHA1-K336R mutant was detected by Western blot analysis. (N) Senescence-associated β-galactosidase (SA-β-gal) staining was assessed in mouse primary PVECs with PDHA1 WT or PDHA1 K336R (scale bar = 20 μm). (O and P) p53, p21, p16, and phosphorylated histone H2AX (γ-H2AX) protein levels in PVECs with PDHA1 WT or PDHA1 K336R were detected by Western blot. n = 3. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Rabbit anti-p-IRF3 S396 antibody , ABclonal , AP0623 , 1: 1,000.

Techniques: De-Phosphorylation Assay, Immunoprecipitation, Western Blot, Mutagenesis, Activity Assay, Phospho-proteomics, Transfection, Expressing, Staining

Pyruvate dehydrogenase E1 component subunit alpha (PDHA1)-activation-driven endothelial senescence via the cyclic GMP-AMP synthase (cGAS) signaling pathway. Cellular senescence in pulmonary vascular endothelial cells (PVECs) was induced by treatment with AZD7545. (A) The mitochondrial reactive oxygen species (mtROS) in AZD7545-treated PVECs were detected by an ROS kit (scale bar = 20 μm). (B and C) JC-1 staining showing mitochondrial membrane potential in endothelial cells (scale bar = 20 μm). (D) Quantification of cytosolic mitochondrial DNA (mtDNA) for the Nd1 , Cytb , and D-loop in AZD7545-treated PVECs was performed by real-time polymerase chain reaction (PCR). (E and F) Western blot and quantification for cGAS, stimulator of interferon genes (STING), p-TBK1 Ser172 , TBK1, p-IRF3 Ser396 , and IRF3 protein expression. (G) Primary PVECs isolated from Cgas WT and Cgas KO mice were stimulated with AZD7545 (40 μM) for 24 h. Senescence-associated β-galactosidase (SA-β-gal) staining was performed to detect AZD7545-induced senescence in primary PVECs from Cgas WT and Cgas KO mice; scale bar = 20 μm. (H) Ki67 staining was performed in AZD7545-treated primary PVECs from Cgas KO mice; scale bar = 50 μm. (I and J) The expression of senescence-related proteins (cGAS, p53, p21, p16, and phosphorylated histone H2AX [γ-H2AX]) was examined by Western blot in AZD7545-treated primary PVECs isolated from Cgas WT and Cgas KO mice. α-Tubulin was used as the internal control. n = 3. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Journal: Research

Article Title: PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence

doi: 10.34133/research.1398

Figure Lengend Snippet: Pyruvate dehydrogenase E1 component subunit alpha (PDHA1)-activation-driven endothelial senescence via the cyclic GMP-AMP synthase (cGAS) signaling pathway. Cellular senescence in pulmonary vascular endothelial cells (PVECs) was induced by treatment with AZD7545. (A) The mitochondrial reactive oxygen species (mtROS) in AZD7545-treated PVECs were detected by an ROS kit (scale bar = 20 μm). (B and C) JC-1 staining showing mitochondrial membrane potential in endothelial cells (scale bar = 20 μm). (D) Quantification of cytosolic mitochondrial DNA (mtDNA) for the Nd1 , Cytb , and D-loop in AZD7545-treated PVECs was performed by real-time polymerase chain reaction (PCR). (E and F) Western blot and quantification for cGAS, stimulator of interferon genes (STING), p-TBK1 Ser172 , TBK1, p-IRF3 Ser396 , and IRF3 protein expression. (G) Primary PVECs isolated from Cgas WT and Cgas KO mice were stimulated with AZD7545 (40 μM) for 24 h. Senescence-associated β-galactosidase (SA-β-gal) staining was performed to detect AZD7545-induced senescence in primary PVECs from Cgas WT and Cgas KO mice; scale bar = 20 μm. (H) Ki67 staining was performed in AZD7545-treated primary PVECs from Cgas KO mice; scale bar = 50 μm. (I and J) The expression of senescence-related proteins (cGAS, p53, p21, p16, and phosphorylated histone H2AX [γ-H2AX]) was examined by Western blot in AZD7545-treated primary PVECs isolated from Cgas WT and Cgas KO mice. α-Tubulin was used as the internal control. n = 3. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Rabbit anti-p-IRF3 S396 antibody , ABclonal , AP0623 , 1: 1,000.

Techniques: Activation Assay, Staining, Membrane, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Isolation, Control

Schematic illustration. Pyruvate dehydrogenase E1 component subunit alpha (PDHA1) activation, driven by S293 dephosphorylation resulting from reduced lactylation at K336, disrupts mitochondrial homeostasis, leading to mitochondrial reactive oxygen species (mtROS)-mediated mitochondrial DNA (mtDNA) release and ultimately triggering cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS–STING)-dependent senescence.

Journal: Research

Article Title: PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence

doi: 10.34133/research.1398

Figure Lengend Snippet: Schematic illustration. Pyruvate dehydrogenase E1 component subunit alpha (PDHA1) activation, driven by S293 dephosphorylation resulting from reduced lactylation at K336, disrupts mitochondrial homeostasis, leading to mitochondrial reactive oxygen species (mtROS)-mediated mitochondrial DNA (mtDNA) release and ultimately triggering cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS–STING)-dependent senescence.

Article Snippet: Rabbit anti-p-IRF3 S396 antibody , ABclonal , AP0623 , 1: 1,000.

Techniques: Activation Assay, De-Phosphorylation Assay

Journal: Research

Article Title: PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence

doi: 10.34133/research.1398

Figure Lengend Snippet: Antibody sources and dilutions

Article Snippet: Rabbit anti-p-IRF3 S396 antibody , ABclonal , AP0623 , 1: 1,000.

Techniques: Western Blot

Renal TECs generate IFN-λ upon RIG-I/MAVS signaling activation. (A) Multiplex immunofluorescence staining for IFN-λ2/3 (red), TECs (E-cadherin, white), fibroblasts (vimentin, cyan), and immune cells (CD45, yellow) in kidney sections at day 7 from sham-operated mice (sham) and UUO mice. Scale bars = 50 μm. Quantification of IFN-λ2/3–positive cells are shown on the right panel ( n = 6). (B–D) Flow cytometry plots showing the purity of isolated E-cadherin + TECs (B), CD45 + immune cells (C), and vimentin + fibroblasts (D) from mouse kidneys ( n = 3). (E) RT-qPCR analysis of Ifn-λ2 and Ifn-λ3 mRNA levels in the indicated purified renal cell populations from sham and UUO mice at day 7 ( n = 4). (F) Western blot analysis of indicated pathway proteins in renal TECs of sham and UUO mice on day 7 ( n = 5 per group). (G–K) WT, Sting –/– (G), Myd88 −/− (H), Trl3 −/− (I), Mda5 −/− (J), and Mavs –/– (K) mice were subjected to sham or UUO surgery ( n = 5 per group). Renal TECs were isolated on day 7 after surgery and analyzed for IFN-λ2/3 and pathway protein expression by western blot (left panels) and Ifn-λ2 and Ifn-λ3 mRNA by RT-qPCR (right panels). (L) Renal TECs from sham and UUO treated with PBS or 50 mg/kg of cFP were analyzed for IFN-λ2/3, p-IRF3, and IRF3 protein levels by western blot (left panel) and Ifn-λ2 and Ifn-λ3 mRNA by RT-qPCR (right panel) ( n = 5 per group). (M) Immunofluorescence staining for IFN-λ2/3 or p-SMAD2/3 in renal TECs (E-cadherin) in kidneys of sham and UUO mice treated with PBS or 50 mg/kg of cFP on day 7 after surgery. Nuclei were counterstained with DAPI. Quantification is shown on the right. n = 4 per group, scale bars = 50 μm. (N) Representative images and quantitative analysis of IFN-λ2/3 or p-SMAD2/3 in renal TECs (E-cadherin) in kidneys of WT and Mavs –/– UUO mice at day 7. n = 4 per group, scale bar = 50 μm. (O) Representative images and quantitative analysis of dsRNA (J2) in renal TECs (E-cadherin) in kidneys of sham and UUO mice at day 7. n = 4 per group, scale bars = 50 μm. (P) ELISA analysis of dsRNA levels in isolated renal TECs. (Q and R) Primary renal TECs were treated with or without 2.5 mM cFP for 6 h, followed by 1 μg/ml of poly(I:C) transfection for 12 h ( n = 3). (Q) Western blot analysis of RIG-I, MAVS, p-IRF3, and IRF3 protein levels. (R) RT-qPCR and ELISA were used to evaluate IFN-λ2/3 mRNA and protein levels, respectively. (S and T) Renal TECs isolated from WT and Mavs –/– mice were transfected with 1 μg/ml of poly(I:C) for 12 h ( n = 3). (S) Western blot analysis of MAVS, p-IRF3, and IRF3 protein levels. (T) IFN-λ2/3 mRNA and protein levels were determined by RT-qPCR and ELISA. Data in A, E, and G–P are pooled from two independent experiments. Data in B–D are pooled from three independent experiments. Data in F and Q–T are representative of three independent experiments. Data are presented as mean ± SEM. ***P < 0.001, ****P < 0.0001, by unpaired two-tailed Student’s t test (A–F and O–P), two-way ANOVA with Tukey’s multiple-comparison test (G–K, N, R, and T), and one-way ANOVA with Tukey’s multiple-comparison test (L and M). ns, no significant difference. Source data are available for this figure: .

Journal: The Journal of Experimental Medicine

Article Title: Interferon-λ drives renal fibrosis by coordinating epithelial–fibroblast crosstalk

doi: 10.1084/jem.20251858

Figure Lengend Snippet: Renal TECs generate IFN-λ upon RIG-I/MAVS signaling activation. (A) Multiplex immunofluorescence staining for IFN-λ2/3 (red), TECs (E-cadherin, white), fibroblasts (vimentin, cyan), and immune cells (CD45, yellow) in kidney sections at day 7 from sham-operated mice (sham) and UUO mice. Scale bars = 50 μm. Quantification of IFN-λ2/3–positive cells are shown on the right panel ( n = 6). (B–D) Flow cytometry plots showing the purity of isolated E-cadherin + TECs (B), CD45 + immune cells (C), and vimentin + fibroblasts (D) from mouse kidneys ( n = 3). (E) RT-qPCR analysis of Ifn-λ2 and Ifn-λ3 mRNA levels in the indicated purified renal cell populations from sham and UUO mice at day 7 ( n = 4). (F) Western blot analysis of indicated pathway proteins in renal TECs of sham and UUO mice on day 7 ( n = 5 per group). (G–K) WT, Sting –/– (G), Myd88 −/− (H), Trl3 −/− (I), Mda5 −/− (J), and Mavs –/– (K) mice were subjected to sham or UUO surgery ( n = 5 per group). Renal TECs were isolated on day 7 after surgery and analyzed for IFN-λ2/3 and pathway protein expression by western blot (left panels) and Ifn-λ2 and Ifn-λ3 mRNA by RT-qPCR (right panels). (L) Renal TECs from sham and UUO treated with PBS or 50 mg/kg of cFP were analyzed for IFN-λ2/3, p-IRF3, and IRF3 protein levels by western blot (left panel) and Ifn-λ2 and Ifn-λ3 mRNA by RT-qPCR (right panel) ( n = 5 per group). (M) Immunofluorescence staining for IFN-λ2/3 or p-SMAD2/3 in renal TECs (E-cadherin) in kidneys of sham and UUO mice treated with PBS or 50 mg/kg of cFP on day 7 after surgery. Nuclei were counterstained with DAPI. Quantification is shown on the right. n = 4 per group, scale bars = 50 μm. (N) Representative images and quantitative analysis of IFN-λ2/3 or p-SMAD2/3 in renal TECs (E-cadherin) in kidneys of WT and Mavs –/– UUO mice at day 7. n = 4 per group, scale bar = 50 μm. (O) Representative images and quantitative analysis of dsRNA (J2) in renal TECs (E-cadherin) in kidneys of sham and UUO mice at day 7. n = 4 per group, scale bars = 50 μm. (P) ELISA analysis of dsRNA levels in isolated renal TECs. (Q and R) Primary renal TECs were treated with or without 2.5 mM cFP for 6 h, followed by 1 μg/ml of poly(I:C) transfection for 12 h ( n = 3). (Q) Western blot analysis of RIG-I, MAVS, p-IRF3, and IRF3 protein levels. (R) RT-qPCR and ELISA were used to evaluate IFN-λ2/3 mRNA and protein levels, respectively. (S and T) Renal TECs isolated from WT and Mavs –/– mice were transfected with 1 μg/ml of poly(I:C) for 12 h ( n = 3). (S) Western blot analysis of MAVS, p-IRF3, and IRF3 protein levels. (T) IFN-λ2/3 mRNA and protein levels were determined by RT-qPCR and ELISA. Data in A, E, and G–P are pooled from two independent experiments. Data in B–D are pooled from three independent experiments. Data in F and Q–T are representative of three independent experiments. Data are presented as mean ± SEM. ***P < 0.001, ****P < 0.0001, by unpaired two-tailed Student’s t test (A–F and O–P), two-way ANOVA with Tukey’s multiple-comparison test (G–K, N, R, and T), and one-way ANOVA with Tukey’s multiple-comparison test (L and M). ns, no significant difference. Source data are available for this figure: .

Article Snippet: The membrane was washed and blocked in TBS plus Tween (TBST) (1 × TBS with 0.05% Tween-20) supplemented with 5% skim milk powder for 1 h at room temperature with gentle shaking, then incubated overnight at 4°C with the following primary antibodies: anti-IFN-λ2/3 (ab191426; Abcam), anti-α-SMA antibody (ab5694; Abcam), anti-fibronectin antibody (ab2413; Abcam), anti-vimentin (A19607; ABclonal), p-STAT1 (9167; Cell Signaling Technology), STAT1 (66545-1-Ig; Proteintech), TGF-β (81746-2-RR; Proteintech), p-SMAD2 (18338; Cell Signaling Technology), p-SMAD3 (9520; Cell Signaling Technology), SMAD2/3 (8685; Cell Signaling Technology), SMAD4 (38454; Cell Signaling Technology), SMAD7 (25840-1-AP; Proteintech), RIG-I (ab302778; Abcam), MAVS (A25005; ABclonal), p-IRF3 (AP0623; ABclonal), IRF3 (MA5-32348; Invitrogen), p-ERK (9101; Cell Signaling Technology), ERK (9102; Cell Signaling Technology), p-JNK (9251; Cell Signaling Technology), JNK (9252; Cell Signaling Technology), p-mTOR (2971; Cell Signaling Technology), mTOR (2983; Cell Signaling Technology), p-p38 (9215; Cell Signaling Technology), p38 (9212; Cell Signaling Technology), p-PI3K (17366; Cell Signaling Technology), PI3K (4257; Cell Signaling Technology), MDA5 (ab315242; Abcam), p-STING (72971; Cell Signaling Tehcnology), STING (13647; Cell Signaling Technology), TLR3 (HA724070; HUABIO), Myd88 (AF7524; Beyotime), and GAPDH (81640-5-RR; Proteintech).

Techniques: Activation Assay, Multiplex Assay, Immunofluorescence, Staining, Flow Cytometry, Isolation, Quantitative RT-PCR, Purification, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Transfection, Two Tailed Test, Comparison

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p irf3 (Cell Signaling Technology Inc)

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