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A Potential Peptide Therapeutic Derived from the Juxtamembrane Domain of the Epidermal Growth Factor Receptor

Figure 7

TE-64562 effects downstream EGFR signaling.

(A) Serum starved MDA-MB-231 cells were treated with TE-64562 (0.6, 1.2, 2.5 5.0 10 and 20 µM), an EGFR specific tyrosine kinase inhibitor (2.0 µM, TKI) or vehicle for 30 minutes, followed by EGF treatment (10 ng/mL) for 10 minutes. Cell lysates were collected and analyzed by Western blot for (A) phospho-Akt (S273), total Akt, phospho-Erk (p44/p42, T202/Y204) and total Erk. Blots were stripped and re-probed for α-tubulin. The Erk (N = 3) and Akt (N = 4) data from separate experiments, all of which are shown in Figure S6, were analyzed. The normalized (ratio of phospho to total intensity) data were plotted as mean values from with the error bars representing the standard error of the mean. The significant differences (*P<0.04) were assessed between each treatment condition and the EGF-treated control (lane 2). (B) Serum starved MDA-MB-231 cells were treated with TE-64562 (0.6, 1.2, 2.5 5.0 10 and 20 µM), an EGFR specific tyrosine kinase inhibitor (2.0 µM, TKI), Tat (20 µM) or vehicle for 30 minutes, followed by EGF treatment (10 ng/mL) for 10 minutes. Results represent one of three independent experiments. Also see Fig. S6. (C) Serum starved MDA-MB-231 cells were treated with TE-64562 (5.0, 10.0 and 20.0 µM) or T-Poly-Ala control peptide (5.0, 10.0 and 20.0 µM) or vehicle for 30 minutes, followed by EGF treatment (10 ng/mL) for 10 minutes. Results are representative of three independent experiments.

Figure 7

doi: https://doi.org/10.1371/journal.pone.0049702.g007