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. 2023 Oct 4;299(11):105319. doi: 10.1016/j.jbc.2023.105319

Figure 2.

Figure 2

PrP KO–induced cellular senescence is regulated by EGFR.A, representative Western blotting of EGFR in WT and KO NSCs (left) and quantification (right). B, schematic showing media and inhibitor manipulations of EGFR signaling carried out for 24 h in C. Image created with BioRender.com. C, relative senescence staining (beta-galactosidase) of WT (left) and PrP KO (right) NSCs following removal of EGF (NoEGF) or addition of the EGFR inhibitor afatinib to block EGFR signaling or doubling of the EGF concentration in the growth to increase EGFR signaling. D, Western blotting (left) and densitometry (right) of MEK2 detection, after 24 h in media with normal, 0, or double EGF concentrations. Results were compared by two-tailed unpaired student’s t test with Welch’s correction (A; n = 4) or by one-way ANOVA compared to control (C, n = 4, and D, n = 3) ∗p < 0.05. Graphs are displayed relative to the average of the WT (A), normal 1× EGF media controls (“Ctrl”; C), or WT Ctrl (D). EGFR, epidermal growth factor receptor; NSC, neural stem cell; PrP, prion protein.