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Bioss p p65 rabbit ab
The mRNA expression of ITGAV, FAK, PLC, PKC, <t>p65,</t> ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.
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The mRNA expression of ITGAV, FAK, PLC, PKC, <t>p65,</t> ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.
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Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Monoclonal Antibody Abmart T58364 Anti Nf κb P65 Monoclonal Antibody Abclonal A19653 Anti P Nf κb P P65, supplied by Abmart Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Affinity Biosciences phosphorylated p65 p p65 antibody
Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, <t>p65,</t> P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Sch B <t>inhibits</t> <t>NF-κB</t> signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of <t>p65</t> expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.
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PUE inhibits the TLR4/MyD88/NF-κB signaling pathway in VaD rats. (A) mRNA levels of TLR4 and MyD88( n = 4); (B) Immunohistochemical staining of P- NF-κB <t>P65</t> in hippocampus (200×, 400×); (C–F) Protein levels of TLR4, Myd88, P- NF-κB P65, NF-κB P65 ( n = 4); Data are presented as mean ± SEM. Significant differences compared with Sham group were designated as * P < 0.05, with Model group as # P < 0.05, with PUE group as & P < 0.05 and with LPS group as △ P < 0.05.
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Image Search Results


The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Article Snippet: p-p65 Rabbit Ab , Bioss , bs-0982R , 1: 1500.

Techniques: Expressing

The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Article Snippet: p-p65 Rabbit Ab , Bioss , bs-0982R , 1: 1500.

Techniques: Activity Assay

Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, p65, P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Journal: Materials Today Bio

Article Title: Ultrasmall Prussian blue–integrated cryogel for enhanced ROS scavenging and immunomodulation via cGAS–STING inhibition in wound healing

doi: 10.1016/j.mtbio.2026.103056

Figure Lengend Snippet: Potential therapeutic mechanism of Cryogel@USPB in wounds. (A) The relative mRNA expression of STING1 and interferon alpha after the treatment of Cryogel@USPB (n = 3). (B) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in diabetic wounds. (C) Immunofluorescent staining of F4/80 (green), STING (red), and DAPI (blue) on day7 in deep second-degree burn wounds. (D) Expression of STING, p-STING, cGAS, IRF3, p-IRF3, p65, P-p65 in three individual skin wound tissues of diabetic mice in the Cryogel@USPB and control group. (E) Expression of STING, p-STING, cGAS, IRF3, P-IRF3, p65, p-p65 in three individual skin tissues of deep second-degree burn wounds in the Cryogel@USPB and control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The primary antibodies were: cGAS (1:1000, Proteintech, USA), STING (1:1000, Proteintech, USA), p-STING (1:1000, Proteintech, USA), IRF3 (1:1000, CST, USA), p-IRF3(1:1000, CST, USA), p65(1:1000, CST, USA ) , p-p65(1:1000, CST, USA ) , GADPH (1:5000, CST, USA) and β-actin (1:5000, CST, USA).

Techniques: Expressing, Staining, Control

Sch B inhibits NF-κB signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of p65 expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

Journal: Oncology Letters

Article Title: Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis

doi: 10.3892/ol.2026.15551

Figure Lengend Snippet: Sch B inhibits NF-κB signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of p65 expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

Article Snippet: p-p65 NF-κB (Ser536) , 3033 , 1:1,000 , Cell Signaling Technology, Inc..

Techniques: Expressing, Luciferase, Immunofluorescence, Staining, Activity Assay

PUE inhibits the TLR4/MyD88/NF-κB signaling pathway in VaD rats. (A) mRNA levels of TLR4 and MyD88( n = 4); (B) Immunohistochemical staining of P- NF-κB P65 in hippocampus (200×, 400×); (C–F) Protein levels of TLR4, Myd88, P- NF-κB P65, NF-κB P65 ( n = 4); Data are presented as mean ± SEM. Significant differences compared with Sham group were designated as * P < 0.05, with Model group as # P < 0.05, with PUE group as & P < 0.05 and with LPS group as △ P < 0.05.

Journal: Frontiers in Pharmacology

Article Title: Investigating the therapeutic mechanism of Puerarin in vascular dementia: an integrated approach combining network pharmacology and experimental validation

doi: 10.3389/fphar.2026.1796295

Figure Lengend Snippet: PUE inhibits the TLR4/MyD88/NF-κB signaling pathway in VaD rats. (A) mRNA levels of TLR4 and MyD88( n = 4); (B) Immunohistochemical staining of P- NF-κB P65 in hippocampus (200×, 400×); (C–F) Protein levels of TLR4, Myd88, P- NF-κB P65, NF-κB P65 ( n = 4); Data are presented as mean ± SEM. Significant differences compared with Sham group were designated as * P < 0.05, with Model group as # P < 0.05, with PUE group as & P < 0.05 and with LPS group as △ P < 0.05.

Article Snippet: Briefly, the sections were pretreated with sodium citrate buffer (Boster Biological Technology, Pleasanton, CA, USA, Cat. No.: AR0024) at 98 °C for 30 min for antigen retrieval, and then the endogenous peroxidase activity was blocked with SignalStain® Peroxidase Blocking Reagent (CST, Danvers, MA, USA, Cat. No.: 15039S) for 10 min and then with BSA (Biyuntian biological technology, Shanghai, China, Cat. No.: ST023) for 30 min, incubated with the primary P-NF-κB p65 (1:300, abmart, Shanghai, China, No.: TP56372) overnight at 4 °C, and finally with goat anti-mouse biotinylated antibody (1:200, CST, Danvers, MA, USA, No.: 14709S) for 30 min at room temperature.

Techniques: Immunohistochemical staining, Staining