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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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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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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.)
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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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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