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. 2010 Apr 6;5(4):e9999. doi: 10.1371/journal.pone.0009999

Figure 10. Inhibition of protein synthesis blocks U18666A-induced increase in RhoA and growth cone collapse.

Figure 10

A&B. Immunoblotting analysis of various proteins in cultured cortical neurons treated with DMSO (D) or U18666A (U) in the presence or absence of the protein synthesis inhibitor ementine (Em). A. Representative images of immunoblots probed with antibodies against ubiquitin (Ubi), phospho-Mdm2 (p-Mdm2), phospho-p38 MAPK (p-p38), phospho-p53 (p-p53), RhoA, phospho LIM Kinase (p-LIMK), and GAPDH (loading control). B. Quantitative data of p-p53Δ, RhoA, and p-LIMK (**p<0.01 as compared to DMSO-treated, ##p<0.01 as compared to U18666A-treated; n = 3–6 from 3 individual experiments). C. Emetine application also significantly reduced U18666A treatment-induced growth cone collapse (n = 100 growth cones; ** p<0.001 as compared to DMSO-treated growth cones and ##p<0.01 as compared to U18666A-treated). D. Treatment with p53 inhibitor, pifithrin-μ (P) induced rapid increase in levels of RhoA and p-LIMK; both events were blocked by emetine (E) treatment.