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p p65 rabbit ab  (Bioss)


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    Structured Review

    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.
    P P65 Rabbit Ab, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 137 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p p65 rabbit ab/product/Bioss
    Average 95 stars, based on 137 article reviews
    p p65 rabbit ab - by Bioz Stars, 2026-05
    95/100 stars

    Images

    1) Product Images from "Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor"

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

    Journal: Poultry Science

    doi: 10.1016/j.psj.2026.106922

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

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: Activity Assay



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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.)
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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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    Cell Signaling Technology Inc p p65 nf κb ser536
    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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    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