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polyclonal rabbit anti mouse p egfr antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc polyclonal rabbit anti mouse p egfr antibody
    Fig. 3. Silibinin modulated the expression of <t>p-EGFR,</t> p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).
    Polyclonal Rabbit Anti Mouse P Egfr Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 4192 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/polyclonal+rabbit+anti+mouse+p+egfr+antibody/EGF+Receptor+Antibody/pm40280368-142-9-15
    Average 97 stars, based on 4192 article reviews
    polyclonal rabbit anti mouse p egfr antibody - by Bioz Stars, 2026-09
    97/100 stars

    Images

    1) Product Images from "Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway."

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.

    Journal: Brain research bulletin

    doi: 10.1016/j.brainresbull.2025.111353

    Fig. 3. Silibinin modulated the expression of p-EGFR, p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).
    Figure Legend Snippet: Fig. 3. Silibinin modulated the expression of p-EGFR, p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).

    Techniques Used: Expressing, Immunohistochemical staining, Staining

    Fig. 4. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 24 h after pMCAO. (A) Representative western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 24 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, n = 6 per group).
    Figure Legend Snippet: Fig. 4. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 24 h after pMCAO. (A) Representative western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 24 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, n = 6 per group).

    Techniques Used: Expressing, Western Blot

    Fig. 5. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 72 h after pMCAO. (A) Representative Western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, *** P < 0.001, n = 6 per group).
    Figure Legend Snippet: Fig. 5. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 72 h after pMCAO. (A) Representative Western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, *** P < 0.001, n = 6 per group).

    Techniques Used: Expressing, Western Blot

    Fig. 8. C225 attenuated the regulatory effects of silibinin on the expression of p-EGFR, p-ERK, and cleaved-Caspase3 in the brain tissue after infarction. (A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post-ischemia. (BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, *P < 0.05, ** P < 0.01, ***P < 0.001; n = 6 per group).
    Figure Legend Snippet: Fig. 8. C225 attenuated the regulatory effects of silibinin on the expression of p-EGFR, p-ERK, and cleaved-Caspase3 in the brain tissue after infarction. (A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post-ischemia. (BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, *P < 0.05, ** P < 0.01, ***P < 0.001; n = 6 per group).

    Techniques Used: Expressing, Immunohistochemical staining, Staining

    Related Articles

    Expressing:

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.
    Article Snippet: They were then incubated with primary antibodies overnight at 4 ◦C.They were then incubated with primary antibodies overnight at 4 ◦C.. The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).. Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.

    Immunohistochemical staining:

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.
    Article Snippet: They were then incubated with primary antibodies overnight at 4 ◦C.They were then incubated with primary antibodies overnight at 4 ◦C.. The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).. Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.

    Staining:

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.
    Article Snippet: They were then incubated with primary antibodies overnight at 4 ◦C.They were then incubated with primary antibodies overnight at 4 ◦C.. The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).. Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.

    Western Blot:

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.
    Article Snippet: They were then incubated with primary antibodies overnight at 4 ◦C.They were then incubated with primary antibodies overnight at 4 ◦C.. The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).. Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.Immunohistochemistry was performed using the avidin-biotin technique, with hematoxylin as the counterstain.



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    Fig. 3. Silibinin modulated the expression of <t>p-EGFR,</t> p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).
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    Image Search Results


    Fig. 3. Silibinin modulated the expression of p-EGFR, p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).

    Journal: Brain research bulletin

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.

    doi: 10.1016/j.brainresbull.2025.111353

    Figure Lengend Snippet: Fig. 3. Silibinin modulated the expression of p-EGFR, p-ERK, cleaved-Caspase3 24 h and 72 h after pMCAO.(A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 24 h post-ischemia.(BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One- Way ANOVA, *P < 0.05, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group). (E) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, and pMCAO + SIL-M groups 72 h post-ischemia. (FGH) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, **P < 0.01, ***P < 0.001, pMCAO + SIL-M group vs. pMCAO group; n = 6 per group).

    Article Snippet: The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).

    Techniques: Expressing, Immunohistochemical staining, Staining

    Fig. 4. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 24 h after pMCAO. (A) Representative western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 24 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, n = 6 per group).

    Journal: Brain research bulletin

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.

    doi: 10.1016/j.brainresbull.2025.111353

    Figure Lengend Snippet: Fig. 4. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 24 h after pMCAO. (A) Representative western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 24 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, n = 6 per group).

    Article Snippet: The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).

    Techniques: Expressing, Western Blot

    Fig. 5. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 72 h after pMCAO. (A) Representative Western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, *** P < 0.001, n = 6 per group).

    Journal: Brain research bulletin

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.

    doi: 10.1016/j.brainresbull.2025.111353

    Figure Lengend Snippet: Fig. 5. Silibinin modulated the expression of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax 72 h after pMCAO. (A) Representative Western blot images of p-EGFR, EGFR, p-ERK, ERK, cleaved-Caspase3, Bcl2 and Bax in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post- ischemia. (BCDEF) Quantitative analysis of p-EGFR/EGFR, p-ERK/ERK, cleaved-Caspase3, Bcl2 and Bax. (One-Way ANOVA, *P < 0.05, ** P < 0.01, *** P < 0.001, n = 6 per group).

    Article Snippet: The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).

    Techniques: Expressing, Western Blot

    Fig. 8. C225 attenuated the regulatory effects of silibinin on the expression of p-EGFR, p-ERK, and cleaved-Caspase3 in the brain tissue after infarction. (A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post-ischemia. (BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, *P < 0.05, ** P < 0.01, ***P < 0.001; n = 6 per group).

    Journal: Brain research bulletin

    Article Title: Silibinin protects the ischemic brain in mice by exerting anti-apoptotic effects via the EGFR/ERK pathway.

    doi: 10.1016/j.brainresbull.2025.111353

    Figure Lengend Snippet: Fig. 8. C225 attenuated the regulatory effects of silibinin on the expression of p-EGFR, p-ERK, and cleaved-Caspase3 in the brain tissue after infarction. (A) Immunohistochemical staining of p-EGFR, p-ERK and cleaved-Caspase3 in the Sham, pMCAO, pMCAO + SIL-M, pMCAO + SIL-M + C225, pMCAO + C225 groups 72 h post-ischemia. (BCD) Quantitative analysis of p-EGFR, p-ERK and cleaved-Caspase3. (One-Way ANOVA, *P < 0.05, ** P < 0.01, ***P < 0.001; n = 6 per group).

    Article Snippet: The primary antibodies, diluted in 0.01 M PBS, included: polyclonal rabbit anti-mouse p-EGFR antibody (1:200, Cell Signaling Technology, USA), polyclonal rabbit anti-mouse p-ERK antibody (1:400, Cell Signaling Technology), and monoclonal rabbit anti-mouse cleaved-Caspase-3 antibody (1:300, Cell Signaling Technology).

    Techniques: Expressing, Immunohistochemical staining, Staining