ma p egfr cell signaling technology Search Results


96
Proteintech phospho egfr
Effects <t>of</t> <t>ERK1/2</t> inhibition (SCH772984; 2 µM), Akt inhibition (MK2206; 2 µM), and dual inhibition (SCH + MK) on Aa-EV-induced migration (n = 6). (D) Effect of the <t>pan-EGFR</t> inhibitor sapitinib (10 µM) on Aa-EV-induced migration (n = 6). Representative microscopy images (left panels) and quantification (right panels) are shown. Scale bars: 500 µm. The data are presented as the means ± SDs. *P < 0.05; **P < 0.01; ***P < 0.001 (Tukey’s test).
Phospho Egfr, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
Santa Cruz Biotechnology p38 mapk antibody
FIG. 4. Ligand-induced apoptosis in SKBr3/EGFR cells. A, SKBr3/EGFR cells were incubated in DMEM containing 5% FBS in 60-mm dishes in the presence of EGF (100 ng/ml), EGF, and <t>p38</t> <t>MAPK</t> inhibitor SB203580 (10 M) or vehicle for 4 days. The DNA ladder samples were prepared as described under “Experimen- tal Procedures.” The right lane represents a positive control from the manufacturer’s kit. B, SKBr3/EGFR cells were grown on Lab-Tek 4-well chamber slides in the presence of EGF, EGF and SB203580, or vehicle for 4 days. The cells were fixed in 4% paraformaldehyde, and DNA frag- mentation was detected as described un- der “Experimental Procedures.” Light mi- croscopy was used to visualize apoptotic cells stained with horseradish peroxidase. C, SKBr3/EGFR cells were grown in 5%FBS, DMEM in the presence of EGF, EGF and SB203580, or vehicle for 5 days. The cells were incubated with 1 g/ml Hoechst 33342 for 30 min. Nuclear stain- ing was visualized using fluorescent mi- croscopy. The arrows indicate apoptotic cells with nuclear fragmentation.
P38 Mapk Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The epidermal growth factor (EGF) receptor is a transmembrane tyrosine kinase that belongs to the HER/ErbB protein family. Ligand binding results in receptor dimerization, autophosphorylation, activation of downstream signaling, internalization, and lysosomal degradation (1,2). Phosphorylation
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Image Search Results


Effects of ERK1/2 inhibition (SCH772984; 2 µM), Akt inhibition (MK2206; 2 µM), and dual inhibition (SCH + MK) on Aa-EV-induced migration (n = 6). (D) Effect of the pan-EGFR inhibitor sapitinib (10 µM) on Aa-EV-induced migration (n = 6). Representative microscopy images (left panels) and quantification (right panels) are shown. Scale bars: 500 µm. The data are presented as the means ± SDs. *P < 0.05; **P < 0.01; ***P < 0.001 (Tukey’s test).

Journal: bioRxiv

Article Title: Periodontal pathogen-derived extracellular vesicles promote EGFR-dependent malignant traits in human pancreatic cancer cells

doi: 10.64898/2026.01.29.700732

Figure Lengend Snippet: Effects of ERK1/2 inhibition (SCH772984; 2 µM), Akt inhibition (MK2206; 2 µM), and dual inhibition (SCH + MK) on Aa-EV-induced migration (n = 6). (D) Effect of the pan-EGFR inhibitor sapitinib (10 µM) on Aa-EV-induced migration (n = 6). Representative microscopy images (left panels) and quantification (right panels) are shown. Scale bars: 500 µm. The data are presented as the means ± SDs. *P < 0.05; **P < 0.01; ***P < 0.001 (Tukey’s test).

Article Snippet: Membranes were probed with primary antibodies against N-cadherin (Cell Signaling Technology #13116), E-cadherin (Cell Signaling Technology #3195), Vimentin (Cell Signaling Technology, #5741), phospho-Smad2/3 (Cell Signaling Technology #8828), phospho-EGFR (Proteintech #30278-1-AP), phospho-ERK1/2 (Proteintech #28733-1-AP), total ERK1/2 (Proteintech #11257-1-AP), phospho-Akt (Proteintech #66444-1-Ig), total Akt (Proteintech #7074), or His-tag (MBL #D291-7).

Techniques: Inhibition, Migration, Microscopy

Aa-derived extracellular vesicles deliver cytolethal distending toxin (Cdt) into human pancreatic cancer cells, inducing DNA damage and enhancing EGFR–ERK/Akt signaling in a TGFβ-independent manner. This signaling cascade promotes epithelial–mesenchymal transition (EMT) and the acquisition of metastatic traits.

Journal: bioRxiv

Article Title: Periodontal pathogen-derived extracellular vesicles promote EGFR-dependent malignant traits in human pancreatic cancer cells

doi: 10.64898/2026.01.29.700732

Figure Lengend Snippet: Aa-derived extracellular vesicles deliver cytolethal distending toxin (Cdt) into human pancreatic cancer cells, inducing DNA damage and enhancing EGFR–ERK/Akt signaling in a TGFβ-independent manner. This signaling cascade promotes epithelial–mesenchymal transition (EMT) and the acquisition of metastatic traits.

Article Snippet: Membranes were probed with primary antibodies against N-cadherin (Cell Signaling Technology #13116), E-cadherin (Cell Signaling Technology #3195), Vimentin (Cell Signaling Technology, #5741), phospho-Smad2/3 (Cell Signaling Technology #8828), phospho-EGFR (Proteintech #30278-1-AP), phospho-ERK1/2 (Proteintech #28733-1-AP), total ERK1/2 (Proteintech #11257-1-AP), phospho-Akt (Proteintech #66444-1-Ig), total Akt (Proteintech #7074), or His-tag (MBL #D291-7).

Techniques: Derivative Assay

FIG. 4. Ligand-induced apoptosis in SKBr3/EGFR cells. A, SKBr3/EGFR cells were incubated in DMEM containing 5% FBS in 60-mm dishes in the presence of EGF (100 ng/ml), EGF, and p38 MAPK inhibitor SB203580 (10 M) or vehicle for 4 days. The DNA ladder samples were prepared as described under “Experimen- tal Procedures.” The right lane represents a positive control from the manufacturer’s kit. B, SKBr3/EGFR cells were grown on Lab-Tek 4-well chamber slides in the presence of EGF, EGF and SB203580, or vehicle for 4 days. The cells were fixed in 4% paraformaldehyde, and DNA frag- mentation was detected as described un- der “Experimental Procedures.” Light mi- croscopy was used to visualize apoptotic cells stained with horseradish peroxidase. C, SKBr3/EGFR cells were grown in 5%FBS, DMEM in the presence of EGF, EGF and SB203580, or vehicle for 5 days. The cells were incubated with 1 g/ml Hoechst 33342 for 30 min. Nuclear stain- ing was visualized using fluorescent mi- croscopy. The arrows indicate apoptotic cells with nuclear fragmentation.

Journal: The Journal of biological chemistry

Article Title: Ligand-induced, p38-dependent apoptosis in cells expressing high levels of epidermal growth factor receptor and ErbB-2.

doi: 10.1074/jbc.M311655200

Figure Lengend Snippet: FIG. 4. Ligand-induced apoptosis in SKBr3/EGFR cells. A, SKBr3/EGFR cells were incubated in DMEM containing 5% FBS in 60-mm dishes in the presence of EGF (100 ng/ml), EGF, and p38 MAPK inhibitor SB203580 (10 M) or vehicle for 4 days. The DNA ladder samples were prepared as described under “Experimen- tal Procedures.” The right lane represents a positive control from the manufacturer’s kit. B, SKBr3/EGFR cells were grown on Lab-Tek 4-well chamber slides in the presence of EGF, EGF and SB203580, or vehicle for 4 days. The cells were fixed in 4% paraformaldehyde, and DNA frag- mentation was detected as described un- der “Experimental Procedures.” Light mi- croscopy was used to visualize apoptotic cells stained with horseradish peroxidase. C, SKBr3/EGFR cells were grown in 5%FBS, DMEM in the presence of EGF, EGF and SB203580, or vehicle for 5 days. The cells were incubated with 1 g/ml Hoechst 33342 for 30 min. Nuclear stain- ing was visualized using fluorescent mi- croscopy. The arrows indicate apoptotic cells with nuclear fragmentation.

Article Snippet: Materials—Monoclonal antibody to the ErbB-2 cytoplasmic domain (Ab3) was from Oncogene Science, polyclonal antibodies to phosphorylated p38 MAPK, MKK3/6, MAPKAPK2, and HSP27 were from Cell Signaling Technology, p38 MAPK antibody and EGFR antibody were from Santa Cruz Biotechnology.

Techniques: Incubation, Positive Control, Staining

FIG. 5. p38 MAPK inhibitor pre- vents ligand-induced apoptosis in SKBr3/EGFR cells. SKBr3/EGFR cells were incubated in 12-well plates in the presence of EGF (100 ng/ml) (gray col- umns), in the presence of EGF (100 ng/ml) and SB203580 (10 M) (black columns), or with vehicle (white columns) for the indi- cated times. The cells were trypsinized in 400 l of 0.25% trypsin, 0.1% EDTA solu- tion and counted using hemacytometer. Results of one (of three) representative experiment are shown.

Journal: The Journal of biological chemistry

Article Title: Ligand-induced, p38-dependent apoptosis in cells expressing high levels of epidermal growth factor receptor and ErbB-2.

doi: 10.1074/jbc.M311655200

Figure Lengend Snippet: FIG. 5. p38 MAPK inhibitor pre- vents ligand-induced apoptosis in SKBr3/EGFR cells. SKBr3/EGFR cells were incubated in 12-well plates in the presence of EGF (100 ng/ml) (gray col- umns), in the presence of EGF (100 ng/ml) and SB203580 (10 M) (black columns), or with vehicle (white columns) for the indi- cated times. The cells were trypsinized in 400 l of 0.25% trypsin, 0.1% EDTA solu- tion and counted using hemacytometer. Results of one (of three) representative experiment are shown.

Article Snippet: Materials—Monoclonal antibody to the ErbB-2 cytoplasmic domain (Ab3) was from Oncogene Science, polyclonal antibodies to phosphorylated p38 MAPK, MKK3/6, MAPKAPK2, and HSP27 were from Cell Signaling Technology, p38 MAPK antibody and EGFR antibody were from Santa Cruz Biotechnology.

Techniques: Incubation

FIG. 7. EGF-induced activation of p38 MAPK pathway in SKBr3/EGFR cells. The cells were incubated in the presence of EGF (100 ng/ml), EGF and SB203580 (10 M), or vehicle for the indicated times. After incubation the cells were lysed, and aliquots containing equal amounts of protein were subjected to 10% SDS-PAGE and West- ern blotting (W.B.) with antibodies to phosphorylated (anti-ph) p38 MAPK, MKK3/6, MAPKAPK2, HSP27. The presence of equal amounts of protein in each sample was confirmed with antibody against total p38 MAPK. A, C, and D show activation of the indicated protein kinases in SKBr3/EGFR cells. B shows the absence of MKK3/6 activation in con- trol SKBr3 cells.

Journal: The Journal of biological chemistry

Article Title: Ligand-induced, p38-dependent apoptosis in cells expressing high levels of epidermal growth factor receptor and ErbB-2.

doi: 10.1074/jbc.M311655200

Figure Lengend Snippet: FIG. 7. EGF-induced activation of p38 MAPK pathway in SKBr3/EGFR cells. The cells were incubated in the presence of EGF (100 ng/ml), EGF and SB203580 (10 M), or vehicle for the indicated times. After incubation the cells were lysed, and aliquots containing equal amounts of protein were subjected to 10% SDS-PAGE and West- ern blotting (W.B.) with antibodies to phosphorylated (anti-ph) p38 MAPK, MKK3/6, MAPKAPK2, HSP27. The presence of equal amounts of protein in each sample was confirmed with antibody against total p38 MAPK. A, C, and D show activation of the indicated protein kinases in SKBr3/EGFR cells. B shows the absence of MKK3/6 activation in con- trol SKBr3 cells.

Article Snippet: Materials—Monoclonal antibody to the ErbB-2 cytoplasmic domain (Ab3) was from Oncogene Science, polyclonal antibodies to phosphorylated p38 MAPK, MKK3/6, MAPKAPK2, and HSP27 were from Cell Signaling Technology, p38 MAPK antibody and EGFR antibody were from Santa Cruz Biotechnology.

Techniques: Activation Assay, Incubation, SDS Page

FIG. 6. EGF-induced activation of p38 MAPK pathway in SKBr3/EGFR cells (A and B) or control SKBr3 cells (C). The cells were incubated in the presence of EGF (100 ng/ml), EGF and SB203580 (10 M), or vehicle for the indicated times. After incubation the cells were lysed, and aliquots containing equal amounts of protein were subjected to 10% SDS-PAGE and Western blotting (W.B.) with antibod- ies to phosphorylated (anti-ph) p38 MAPK. The presence of equal amounts of protein in each sample was confirmed with antibody against total p38 MAPK.

Journal: The Journal of biological chemistry

Article Title: Ligand-induced, p38-dependent apoptosis in cells expressing high levels of epidermal growth factor receptor and ErbB-2.

doi: 10.1074/jbc.M311655200

Figure Lengend Snippet: FIG. 6. EGF-induced activation of p38 MAPK pathway in SKBr3/EGFR cells (A and B) or control SKBr3 cells (C). The cells were incubated in the presence of EGF (100 ng/ml), EGF and SB203580 (10 M), or vehicle for the indicated times. After incubation the cells were lysed, and aliquots containing equal amounts of protein were subjected to 10% SDS-PAGE and Western blotting (W.B.) with antibod- ies to phosphorylated (anti-ph) p38 MAPK. The presence of equal amounts of protein in each sample was confirmed with antibody against total p38 MAPK.

Article Snippet: Materials—Monoclonal antibody to the ErbB-2 cytoplasmic domain (Ab3) was from Oncogene Science, polyclonal antibodies to phosphorylated p38 MAPK, MKK3/6, MAPKAPK2, and HSP27 were from Cell Signaling Technology, p38 MAPK antibody and EGFR antibody were from Santa Cruz Biotechnology.

Techniques: Activation Assay, Control, Incubation, SDS Page, Western Blot