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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Cell Signaling Technology Inc anti-perk antibody
Figure 2. FLNa knockdown promotes EGF‑induced <t>EGFR/Akt/ERK</t> phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, <t>phosphorylated.</t>
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Image Search Results


Figure 2. FLNa knockdown promotes EGF‑induced EGFR/Akt/ERK phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, phosphorylated.

Journal: Molecular medicine reports

Article Title: Filamin A regulates EGFR/ERK/Akt signaling and affects colorectal cancer cell growth and migration.

doi: 10.3892/mmr.2019.10622

Figure Lengend Snippet: Figure 2. FLNa knockdown promotes EGF‑induced EGFR/Akt/ERK phosphorylation in SW480 cells. SW480 cells were transfected with shFLNa or control shRNA for 24 h. Then cells were treated with or without EGF (20 nM) for 0, 5, 10 and 30 min. (A) Total proteins were extracted and subjected to western blotting with antibodies against FLNa, EGFR, p‑EGFR, p‑Akt, Akt, p‑ERK and ERK; β‑actin is shown here as a loading control. (B) Band intensities for the ratio of FLN/β‑actin were measured. (C) Band intensities for the ratio of p‑EGFR/EGFR, (D) p‑Akt/Akt and (E) p‑ERK/ERK were measured and normalized to β‑actin. **P<0.01 vs. SW480/Ctrl. FLNa, Filamin A; EGF, epidermal growth factor; sh, short hairpin; EGFR, epidermal growth factor receptor; p‑, phosphorylated.

Article Snippet: Primary antibodies included the following: rabbit anti-Flna antibody (1:1,000; cat. no. MaB1680; eMd Millipore), rabbit anti-eGFr antibody (1:1,000; cat. no. 18986-1-aP; ProteinTech Group, inc.), rabbit anti-phosphorylated (p-)eGFr antibody (Tyr1068; 1:2,000; cat. no. 3777; cell Signaling Technology, inc.), rabbit anti-akt antibody (1:1,000; cat. no. 10176-2-aP; ProteinTech Group, inc.), rabbit anti-p-akt antibody (Ser473; 1:1,000; cat. no. 66444-1-ig; ProteinTech Group, inc.), rabbit anti-erK1/2 antibody (1:4,000; cat. no. 16443-1-aP; ProteinTech Group, inc.), rabbit anti-p-erK1/2 antibody (Thr202/Tyr204; 1:3,000; cat. no. 4370, cell Signaling Technology.) and mouse anti-β-actin antibody (1:5,000; cat. no. 60008-1-ig; ProteinTech Group, inc.).

Techniques: Knockdown, Phospho-proteomics, Transfection, Control, shRNA, Western Blot