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    • p egfr  (Novus Biologicals)
    86
    Novus Biologicals p egfr
    P Egfr, supplied by Novus Biologicals, 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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    Average 86 stars, based on 1 article reviews
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    p egfr  (GE Healthcare)
    97
    GE Healthcare p egfr
    P Egfr, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p egfr  (Cell Signaling Technology Inc)
    86
    Cell Signaling Technology Inc p egfr
    A). ST6GAL1 was stably knocked-down (KD) in cells with high endogenous ST6GAL1 expression (MiaPaCa-2, S2-013, S2-LM7AA, OVCAR-3, and OVCAR-5) using lentivirus encoding an shRNA sequence targeting ST6GAL1. As controls, cells were either transduced with lentivirus containing shRNA targeting GFP (shC) or with an empty vector (EV) construct. B). Cells with undetectable endogenous ST6GAL1 (SW48 and OV4) were stably transduced with ST6GAL1-encoding cDNA to overexpress (OE) the enzyme, or with an EV construct. All cell lines represent polyclonal populations. C). Cells with or without ST6GAL1 KD were treated with 100 ng/mL EGF for 15 minutes and immunoblotted <t>for</t> <t>p-EGFR</t> (pY1068) and total EGFR (t-EGFR). D). Cells with or without ST6GAL1 OE were treated with 100 ng/mL EGF for 15 minutes and immunoblotted for p-EGFR and t-EGFR.
    P Egfr, supplied by Cell Signaling Technology 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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    p egfr  (Abcam)
    86
    Abcam p egfr
    Correlation between protein level and tumor response
    P Egfr, supplied by Abcam, 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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    Image Search Results


    A). ST6GAL1 was stably knocked-down (KD) in cells with high endogenous ST6GAL1 expression (MiaPaCa-2, S2-013, S2-LM7AA, OVCAR-3, and OVCAR-5) using lentivirus encoding an shRNA sequence targeting ST6GAL1. As controls, cells were either transduced with lentivirus containing shRNA targeting GFP (shC) or with an empty vector (EV) construct. B). Cells with undetectable endogenous ST6GAL1 (SW48 and OV4) were stably transduced with ST6GAL1-encoding cDNA to overexpress (OE) the enzyme, or with an EV construct. All cell lines represent polyclonal populations. C). Cells with or without ST6GAL1 KD were treated with 100 ng/mL EGF for 15 minutes and immunoblotted for p-EGFR (pY1068) and total EGFR (t-EGFR). D). Cells with or without ST6GAL1 OE were treated with 100 ng/mL EGF for 15 minutes and immunoblotted for p-EGFR and t-EGFR.

    Journal: bioRxiv

    Article Title: Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics

    doi: 10.1101/2023.06.03.543566

    Figure Lengend Snippet: A). ST6GAL1 was stably knocked-down (KD) in cells with high endogenous ST6GAL1 expression (MiaPaCa-2, S2-013, S2-LM7AA, OVCAR-3, and OVCAR-5) using lentivirus encoding an shRNA sequence targeting ST6GAL1. As controls, cells were either transduced with lentivirus containing shRNA targeting GFP (shC) or with an empty vector (EV) construct. B). Cells with undetectable endogenous ST6GAL1 (SW48 and OV4) were stably transduced with ST6GAL1-encoding cDNA to overexpress (OE) the enzyme, or with an EV construct. All cell lines represent polyclonal populations. C). Cells with or without ST6GAL1 KD were treated with 100 ng/mL EGF for 15 minutes and immunoblotted for p-EGFR (pY1068) and total EGFR (t-EGFR). D). Cells with or without ST6GAL1 OE were treated with 100 ng/mL EGF for 15 minutes and immunoblotted for p-EGFR and t-EGFR.

    Article Snippet: Membranes were then probed with antibodies for t-EGFR (1:1000, Cell Signaling Technologies, 4267), p-EGFR (1:1000, pTyr1068, Cell Signaling Technologies, 3777), t-AKT (1:1000, Cell Signaling Technologies, 4691), p-AKT (1:1000, pSer473, Cell Signaling Technologies, 4060), t-NF-κB p65 (1:1000, Cell Signaling Technologies, 8242), p-NF-κB p65 (1:500, pSer536, Cell Signaling Technologies, 3033), t-ERK1/2 (1:1000, Cell Signaling Technologies, 4695) and p-ERK1/2 (1:1000, p-Thr202/p-Tyr204, Cell Signaling Technologies, 4377).

    Techniques: Stable Transfection, Expressing, shRNA, Sequencing, Transduction, Plasmid Preparation, Construct

    OVCAR-3 and OVCAR-5 cells were treated with 100 ng/mL of EGF for 10 minutes, fixed, permeabilized, stained with SNA and/or p-EGFR, and then analyzed by flow cytometry. A). Histograms depicting intracellular staining for p-EGFR before and after treatment with EGF. B). Schematic of the gating strategy. The 10% of cells with the lowest levels of α2,6 sialylation were designated as “SNA low”, and the 10% of cells with the highest levels of α2,6 sialylation were designated as “SNA high”. SNA high and SNA low cells were assessed for levels of p-EGFR. C-D). p-EGFR levels in OVCAR-3 SNA high and SNA low cells. Representative experiment in (C) and quantification in (D). E-F). p-EGFR levels in OVCAR-5 SNA high and SNA low cells. Representative experiment in (E); quantification in (F). Dotted lines indicate the highest peak of the histograms. Graphs depict the MFI +/- S.D. from three independent experiments. (not significant, ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001) as measured by a two-way ANOVA followed by Šidák’s multiple comparison test.

    Journal: bioRxiv

    Article Title: Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics

    doi: 10.1101/2023.06.03.543566

    Figure Lengend Snippet: OVCAR-3 and OVCAR-5 cells were treated with 100 ng/mL of EGF for 10 minutes, fixed, permeabilized, stained with SNA and/or p-EGFR, and then analyzed by flow cytometry. A). Histograms depicting intracellular staining for p-EGFR before and after treatment with EGF. B). Schematic of the gating strategy. The 10% of cells with the lowest levels of α2,6 sialylation were designated as “SNA low”, and the 10% of cells with the highest levels of α2,6 sialylation were designated as “SNA high”. SNA high and SNA low cells were assessed for levels of p-EGFR. C-D). p-EGFR levels in OVCAR-3 SNA high and SNA low cells. Representative experiment in (C) and quantification in (D). E-F). p-EGFR levels in OVCAR-5 SNA high and SNA low cells. Representative experiment in (E); quantification in (F). Dotted lines indicate the highest peak of the histograms. Graphs depict the MFI +/- S.D. from three independent experiments. (not significant, ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001) as measured by a two-way ANOVA followed by Šidák’s multiple comparison test.

    Article Snippet: Membranes were then probed with antibodies for t-EGFR (1:1000, Cell Signaling Technologies, 4267), p-EGFR (1:1000, pTyr1068, Cell Signaling Technologies, 3777), t-AKT (1:1000, Cell Signaling Technologies, 4691), p-AKT (1:1000, pSer473, Cell Signaling Technologies, 4060), t-NF-κB p65 (1:1000, Cell Signaling Technologies, 8242), p-NF-κB p65 (1:500, pSer536, Cell Signaling Technologies, 3033), t-ERK1/2 (1:1000, Cell Signaling Technologies, 4695) and p-ERK1/2 (1:1000, p-Thr202/p-Tyr204, Cell Signaling Technologies, 4377).

    Techniques: Staining, Flow Cytometry

    OV4 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes, or left untreated (-), and then cell lysates were immunoblotted for signaling molecules. A-B). Representative blot (A) and quantification (B) of p-EGFR and t-EGFR. C-D). Representative blot (C) and quantification (D) of p-AKT and t-AKT. E-F). Representative blot (E) and quantification (F) of p-NFκB p65 and t-NFκB p65. G-H). Representative blot (G) and quantification (H) of p-ERK1/2 and t-ERK1/2. Blots from three independent cell lysates were analyzed by densitometry and the phospho to total ratio (p/t) was calculated and normalized to β-tubulin. D.U. = densitometry units. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Journal: bioRxiv

    Article Title: Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics

    doi: 10.1101/2023.06.03.543566

    Figure Lengend Snippet: OV4 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes, or left untreated (-), and then cell lysates were immunoblotted for signaling molecules. A-B). Representative blot (A) and quantification (B) of p-EGFR and t-EGFR. C-D). Representative blot (C) and quantification (D) of p-AKT and t-AKT. E-F). Representative blot (E) and quantification (F) of p-NFκB p65 and t-NFκB p65. G-H). Representative blot (G) and quantification (H) of p-ERK1/2 and t-ERK1/2. Blots from three independent cell lysates were analyzed by densitometry and the phospho to total ratio (p/t) was calculated and normalized to β-tubulin. D.U. = densitometry units. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Article Snippet: Membranes were then probed with antibodies for t-EGFR (1:1000, Cell Signaling Technologies, 4267), p-EGFR (1:1000, pTyr1068, Cell Signaling Technologies, 3777), t-AKT (1:1000, Cell Signaling Technologies, 4691), p-AKT (1:1000, pSer473, Cell Signaling Technologies, 4060), t-NF-κB p65 (1:1000, Cell Signaling Technologies, 8242), p-NF-κB p65 (1:500, pSer536, Cell Signaling Technologies, 3033), t-ERK1/2 (1:1000, Cell Signaling Technologies, 4695) and p-ERK1/2 (1:1000, p-Thr202/p-Tyr204, Cell Signaling Technologies, 4377).

    Techniques:

    OVCAR-3 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes or left untreated (-) and then cell lysates were immunoblotted for signaling molecules. A-B). p-EGFR and t-EGFR. C-D). p-AKT and t-AKT. E-F). p-NFκB p65 and t-NFκB p65. G-H). p-ERK1/2 and t-ERK1/2. The phospho to total ratio (p/t) was calculated and normalized to β-tubulin (“Relative D.U.”). Graphs depict the mean +/- S.D. for three independent immunoblots for each signaling molecule. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Journal: bioRxiv

    Article Title: Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics

    doi: 10.1101/2023.06.03.543566

    Figure Lengend Snippet: OVCAR-3 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes or left untreated (-) and then cell lysates were immunoblotted for signaling molecules. A-B). p-EGFR and t-EGFR. C-D). p-AKT and t-AKT. E-F). p-NFκB p65 and t-NFκB p65. G-H). p-ERK1/2 and t-ERK1/2. The phospho to total ratio (p/t) was calculated and normalized to β-tubulin (“Relative D.U.”). Graphs depict the mean +/- S.D. for three independent immunoblots for each signaling molecule. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Article Snippet: Membranes were then probed with antibodies for t-EGFR (1:1000, Cell Signaling Technologies, 4267), p-EGFR (1:1000, pTyr1068, Cell Signaling Technologies, 3777), t-AKT (1:1000, Cell Signaling Technologies, 4691), p-AKT (1:1000, pSer473, Cell Signaling Technologies, 4060), t-NF-κB p65 (1:1000, Cell Signaling Technologies, 8242), p-NF-κB p65 (1:500, pSer536, Cell Signaling Technologies, 3033), t-ERK1/2 (1:1000, Cell Signaling Technologies, 4695) and p-ERK1/2 (1:1000, p-Thr202/p-Tyr204, Cell Signaling Technologies, 4377).

    Techniques: Western Blot

    OVCAR-5 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes or left untreated (-), and then cell lysates were immunoblotted for signaling molecules. A-B). p-EGFR and t-EGFR. C-D). p-AKT and t-AKT. E-F). p-NFκB p65 and t-NFκB p65. G-H). p-ERK1/2 and t-ERK1/2. The phospho to total ratio (p/t) was calculated and normalized to β-tubulin (“Relative D.U.”). Graphs depict the mean +/- S.D. for three independent immunoblots for each signaling molecule. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Journal: bioRxiv

    Article Title: Sialylation of EGFR by ST6GAL1 induces receptor activation and modulates trafficking dynamics

    doi: 10.1101/2023.06.03.543566

    Figure Lengend Snippet: OVCAR-5 cells were treated with 100 ng/mL of EGF for 5, 15, or 30 minutes or left untreated (-), and then cell lysates were immunoblotted for signaling molecules. A-B). p-EGFR and t-EGFR. C-D). p-AKT and t-AKT. E-F). p-NFκB p65 and t-NFκB p65. G-H). p-ERK1/2 and t-ERK1/2. The phospho to total ratio (p/t) was calculated and normalized to β-tubulin (“Relative D.U.”). Graphs depict the mean +/- S.D. for three independent immunoblots for each signaling molecule. Statistics were calculated using a two-way ANOVA followed by Šidák’s multiple comparison test. (ns: p > 0.05, *: p < 0.05, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001).

    Article Snippet: Membranes were then probed with antibodies for t-EGFR (1:1000, Cell Signaling Technologies, 4267), p-EGFR (1:1000, pTyr1068, Cell Signaling Technologies, 3777), t-AKT (1:1000, Cell Signaling Technologies, 4691), p-AKT (1:1000, pSer473, Cell Signaling Technologies, 4060), t-NF-κB p65 (1:1000, Cell Signaling Technologies, 8242), p-NF-κB p65 (1:500, pSer536, Cell Signaling Technologies, 3033), t-ERK1/2 (1:1000, Cell Signaling Technologies, 4695) and p-ERK1/2 (1:1000, p-Thr202/p-Tyr204, Cell Signaling Technologies, 4377).

    Techniques: Western Blot

    Correlation between protein level and tumor response

    Journal: Journal of Thoracic Disease

    Article Title: A subset of esophageal squamous cell carcinoma patient-derived xenografts respond to cetuximab, which is predicted by high EGFR expression and amplification

    doi: 10.21037/jtd.2018.09.18

    Figure Lengend Snippet: Correlation between protein level and tumor response

    Article Snippet: For all of the samples, the relative EGFR protein expression level was determined by immunohistochemistry (IHC), anti-human antibodies including EGFR (CST, Beverly, MA, USA), P-EGFR (Abcam, Cambridge, MA, USA), HER3 (CST, Beverly, MA, USA), P-HER3 (CST, Beverly, MA, USA), MET (CST, Beverly, MA, USA), P-MET (CST, Beverly, MA, USA), Akt (CST, Beverly, MA, USA), P-Akt (CST, Beverly, MA, USA), ERK (CST, Beverly, MA, USA), P-ERK (CST, Beverly, MA, USA) were applied to stain the positive sections.

    Techniques: Expressing

    Typical EGFR and Akt staining of score 0–3+. EGFR and Akt staining as determined by immunohistochemistry. Panels show representative examples of esophageal tumor specimens stained for total EGFR (A) and Akt (B). EGFR, epidermal growth factor receptor.

    Journal: Journal of Thoracic Disease

    Article Title: A subset of esophageal squamous cell carcinoma patient-derived xenografts respond to cetuximab, which is predicted by high EGFR expression and amplification

    doi: 10.21037/jtd.2018.09.18

    Figure Lengend Snippet: Typical EGFR and Akt staining of score 0–3+. EGFR and Akt staining as determined by immunohistochemistry. Panels show representative examples of esophageal tumor specimens stained for total EGFR (A) and Akt (B). EGFR, epidermal growth factor receptor.

    Article Snippet: For all of the samples, the relative EGFR protein expression level was determined by immunohistochemistry (IHC), anti-human antibodies including EGFR (CST, Beverly, MA, USA), P-EGFR (Abcam, Cambridge, MA, USA), HER3 (CST, Beverly, MA, USA), P-HER3 (CST, Beverly, MA, USA), MET (CST, Beverly, MA, USA), P-MET (CST, Beverly, MA, USA), Akt (CST, Beverly, MA, USA), P-Akt (CST, Beverly, MA, USA), ERK (CST, Beverly, MA, USA), P-ERK (CST, Beverly, MA, USA) were applied to stain the positive sections.

    Techniques: Staining, Immunohistochemistry

    The cetuximab response was significantly correlated with both EGFR amplification and t-EGFR IHC

    Journal: Journal of Thoracic Disease

    Article Title: A subset of esophageal squamous cell carcinoma patient-derived xenografts respond to cetuximab, which is predicted by high EGFR expression and amplification

    doi: 10.21037/jtd.2018.09.18

    Figure Lengend Snippet: The cetuximab response was significantly correlated with both EGFR amplification and t-EGFR IHC

    Article Snippet: For all of the samples, the relative EGFR protein expression level was determined by immunohistochemistry (IHC), anti-human antibodies including EGFR (CST, Beverly, MA, USA), P-EGFR (Abcam, Cambridge, MA, USA), HER3 (CST, Beverly, MA, USA), P-HER3 (CST, Beverly, MA, USA), MET (CST, Beverly, MA, USA), P-MET (CST, Beverly, MA, USA), Akt (CST, Beverly, MA, USA), P-Akt (CST, Beverly, MA, USA), ERK (CST, Beverly, MA, USA), P-ERK (CST, Beverly, MA, USA) were applied to stain the positive sections.

    Techniques: Amplification