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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Clin Cancer Res. 2012 Jan 10;18(5):1472–1482. doi: 10.1158/1078-0432.CCR-11-2906

Figure 1. Identification and characterization of a novel ALK Kinase domain mutation in patients.

Figure 1

Surface (A) and ribbon (B) models of the ALK kinase domain in complex with crizotinib (PDB 2XP2). Insets to the right represent a magnified view of the ATP- binding pocket where crizotinib is located. (A) and (B) were generated using the PyMol molecular graphics system. (C) Ba/F3 cells expressing wild-type EML4-ALK (E6;A20), or the same EML4-ALK construct with the specified ALK kinase domain mutations or empty vector were treated with the indicated concentration of crizotinib and viable cells were measured after 72 hours and then plotted relative to untreated controls. Ba/F3 cells expressing empty vector were grown in the presence of IL-3. (D) SDS-PAGE and immunoblotting analysis to detect the indicated proteins in cell lysates from NIH3T3 cells expressing wild-type EML4-ALK (E6;A20) and EML4-ALK (E6;A20) G1269A treated with the indicated doses of crizotinib for 5 hours. NIH3T3 with empty vector are also shown as a control. (E) Quantitation of western blot in (D) is graphically represented using LiCor image analysis software. (F) Ba/F3 cells expressing wild-type EML4-ALK (E6;A20), or the same EML4-ALK construct with the specified ALK kinase domain mutations or empty vector (with and without IL-3) were plated and viable cells were measured at the indicated time points and plotted.