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p egfr polyclonal antibody  (Proteintech)


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    Structured Review

    Proteintech p egfr polyclonal antibody
    P Egfr Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 121 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+egfr+polyclonal+antibody/10__1016_slash_j__molstruc__2026__145923-234-57-80?v=Proteintech
    Average 94 stars, based on 121 article reviews
    p egfr polyclonal antibody - by Bioz Stars, 2026-07
    94/100 stars

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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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    Figure 5. Activation of <t>p-EGFR</t> in T84 IEC in response to EVs. (A) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to BL23 EVs and epidermal growth factor (EGF). (B) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using one-way ANOVA followed by a Dunnett’s post test compared to the corresponding Controls at 30 min and 60 min, *p < 0.05. (C) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to purified P40 and P75 when stimulated during 1 h. (D) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using student’s t-test, #p < 0.05 compared to Control.
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    Figure 5. Activation of <t>p-EGFR</t> in T84 IEC in response to EVs. (A) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to BL23 EVs and epidermal growth factor (EGF). (B) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using one-way ANOVA followed by a Dunnett’s post test compared to the corresponding Controls at 30 min and 60 min, *p < 0.05. (C) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to purified P40 and P75 when stimulated during 1 h. (D) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using student’s t-test, #p < 0.05 compared to Control.
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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

    Journal: iScience

    Article Title: A desmosomal cadherin controls multipotent hair follicle stem cell quiescence and orchestrates regeneration through adhesion signaling

    doi: 10.1016/j.isci.2023.108568

    Figure Lengend Snippet:

    Article Snippet: Rabbit polyclonal anti-p-EGFR (Tyr845) for immunoblot (1:500 dilution) , Cell Signaling Technology , Cat#2231S; RRID: AB_1264155.

    Techniques: Western Blot, Immunolabeling, Plasmid Preparation, Recombinant, Blocking Assay, Staining, Software, Flow Cytometry, Microscopy, Imaging

    Figure 5. Activation of p-EGFR in T84 IEC in response to EVs. (A) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to BL23 EVs and epidermal growth factor (EGF). (B) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using one-way ANOVA followed by a Dunnett’s post test compared to the corresponding Controls at 30 min and 60 min, *p < 0.05. (C) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to purified P40 and P75 when stimulated during 1 h. (D) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using student’s t-test, #p < 0.05 compared to Control.

    Journal: Scientific reports

    Article Title: Lactobacillus casei extracellular vesicles stimulate EGFR pathway likely due to the presence of proteins P40 and P75 bound to their surface.

    doi: 10.1038/s41598-020-75930-9

    Figure Lengend Snippet: Figure 5. Activation of p-EGFR in T84 IEC in response to EVs. (A) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to BL23 EVs and epidermal growth factor (EGF). (B) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using one-way ANOVA followed by a Dunnett’s post test compared to the corresponding Controls at 30 min and 60 min, *p < 0.05. (C) Expression of p-EGFR, p-Akt and p-ERK 1/2 in response to purified P40 and P75 when stimulated during 1 h. (D) Graphs represent the quantification of p-EGFR, p-Akt and p-ERK1/2. Statistical analysis was performed using student’s t-test, #p < 0.05 compared to Control.

    Article Snippet: Rabbit polyclonal anti-P40N, anti-P75N28, mouse—monoclonal anti-β-actin (Ref. A-2228, Sigma-Aldrich) were diluted 1:5.000 in 5% (w/v) non-fat dry milk in TBS-T and incubated for 2 h, rabbit polyclonal antibodies anti-p-EGFR (Tyr1068, #2234, Cell Signaling), anti-p-Akt (Ser473, #9271, Cell Signaling) and anti-p-Erk1/2 (Thr202/Tyr204, #9101, Cell Signaling) were incubated O/N at 4 °C in 5% BSA in TBS-T. Blots were incubated with secondary goat anti-rabbit and anti-mouse (β-actin) HRP-conjugated antibodies and signals were detected using the ECL advance chemiluminescent reagents as described by the supplier (GE Healthcare).

    Techniques: Activation Assay, Expressing, Purification, Control