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. Author manuscript; available in PMC: 2013 Oct 8.
Published in final edited form as: Biochem Pharmacol. 2011 Feb 1;81(7):881–890. doi: 10.1016/j.bcp.2011.01.017

Figure 2. MLN8237 inhibits Aurora A and B kinase activity and promotes polyploidy.

Figure 2

Figure 2

Figure 2

(A) Interactive docking studies of MLN8237 with the crystal structures of the active forms of Aurora A (color by atom type) and B (green) show binding mode and score that predicts for MLN8237 to interact with both enzyme active sites with Aurora A > B. (B) Granta-519 and SUDHL-4 cells were synchronized with nocodazole without or with various concentrations of MLN8237 for 16 h. pThr288, Aurora A, pHisH3 (Ser10) and HisH3 were analyzed by Western blotting. GAPDH and β-actin were used as loading controls. (C) MLN8237 treatment results in cellular phenotypes consistent with Aurora A deficiency. Top, DNA profiles of MDA-MB-231 and Granta-4 cells treated with vehicle or MLN8237 at 2 μM for 72 h and evaluated by flow cytometry. Bottom, MDA-MB-231 and Granta-4 cells were transfected or infected by Aurora A siRNA or shRNA lentiviral particles, respectively and DNA contents were analyzed by flow cytometry at 96 h. Inset: The levels of Aurora A expression was determined for control and Aurora A knock-down cells by Western blotting analysis.