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. 2019 Dec 30;117(2):1027–1035. doi: 10.1073/pnas.1913054117

Fig. 5.

Fig. 5.

Dysregulation of Ect2 by recurring cancer-associated mutations. (A) Recurring cancer-associated mutations (in red) mapped to the structure of Ect2. The residues tested in this study are shown as spheres. The boxed region is enlarged for further analysis in D. (B) Relative GEF activity of WT and the cancer-associated mutants of Ect2. Error bars indicate SD (n = 3 independent experiments). (C) Cytokinesis defects caused by 3 cancer-associated mutant Ect2. (D) Structure of Ect2 around Arg639. (E) In vitro cell proliferation assays with A375 cells expressing WT (triangles) or R639Q (circles) mutant Ect2. Error bars indicate SD (n = 3 independent experiments). *P < 0.05. (F) Soft agar colony formation assays of A375 cells expressing WT or R639Q mutant Ect2. Error bars indicate SD (n = 3 independent experiments). **P < 0.01. (G) Xenograft tumor models with A375 cells expressing WT or R639Q mutant Ect2. Tumor weights were analyzed after 4-wk inoculation. **P < 0.01.