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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Mol Cancer Ther. 2015 Aug 24;14(11):2576–2585. doi: 10.1158/1535-7163.MCT-15-0443

Fig. 1.

Fig. 1

Effects of individual CP110 phosphorylation sites on Cdk2-inhibition-mediated anaphase catastrophe in murine lung cancer cells. (A) ED-1 cells were transfected with the CP110-MUT expressing vector with the indicated phosphorylation sites restored to wild-type sequences. Twenty-four hours after transfection, cells were treated with seliciclib (10μM) for 24 hours and fixed and scored for multipolar anaphases. (B) Transfection effects of CP110-MUT with both Ser 170 and Thr 194 restored to wild-type sequences on CDK2-inhibition-mediated anaphase catastrophe in ED-1 cells. (C) Transfection effects of CP110-WT expressing vector having Ser 170 and Thr 194 individually or together replaced with alanine residues on CDK2-inhibition-mediated anaphase catastrophe in ED-1 cells. (D) Schematic of CP110-WT, CP110-MUT (8 sites) and CP110-MUT with Ser 170 and Thr 194 restored to wild-type sequences. All experiments were independently replicated at least three times.