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Figure 5. In-cell RTK activity profiling with BCR-ABL and EGFR inhibitors. ; (A) Activity of BCR-ABL inhibitors ponatinib (Pona.), imatinib (Ima.), dasatinib (Dasa.), bosutinib (Bosu.), and nilotinib (Nilo.) against 28 wild-type RTKs, evaluated in 293T cells transfected with RTKs and treated with inhibitors for 20–24 hr. The panel compiles data from immunoblot detections of activated RTKs, each treated with inhibitor concentrations derived from the experiments shown in Figure 5—figure supplement 1. Only one concentration is shown for nilotinib due to its cell toxicity at higher concentrations. Asterisks highlight the previously unreported nilotinib targets LTK and INSR (Supplementary file 1E; Figure 5—figure supplement 1). (B) Activity profiling of 30 wild-type (wt) RTKs and 116 of their active mutants in the presence of 0.5 µM osimertinib. 293T cells were transfected with RTK vectors together with pKrox24(2xD-E_inD)Luc24 hr before osimertinib treatment (for 24 hr). The colors reflect the osimertinib-mediated inhibition of pKrox24(2xD-E_inD)Luctrans-activation induced by a given RTK, relative to cells untreated with osimertinib. Basal levels of osimetrinib-mediated inhibition of pKrox24(2xD-E_inD)Luc were obtained from cells transfected with empty plasmid and then subtracted from the data. (C) 293T cells were transfected with wt LTK or its mutants, and treated with osimertinib (Osi.) for 24 hr. The LTK autophosphorylation (p) reflect LTK activity. Total LTK and actin serve as loading controls. (D) Cell-free kinase assays were carried out with recombinant LTK or EGFR and osimertinib added to the kinase reaction. Phosphorylation (p) of a recombinant STAT1 and autophosphorylation was used to detect LTK and EGFR activation, respectively. Samples with omitted ATP serve as negative controls for kinase activity.

2017

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Figure 5—figure supplement 1. Analyses of cytotoxicity and kinase activities of BCR-ABL and EGFR inhibitors. ; (A) 293T cells were treated with ponatinib, imatinib, dasatinib, bosutinib, nilotinib and osimertinib for 24 hr and the cell amounts were determined by cell counting. Data represent average from three independent experiments (two biological replicates for each point in every experiment) with indicated SD. 0, cells treated with TKI vehicle DMSO. With exception of dasatinib, the inhibitors did not affect 293T proliferation at the concentration ranges (red lines) used in RTK screening (Figure 5A). (B, C) Cells were transfected with human wild-type ABL, and p190 and p210 variants of BCR-ABL, and wild-type human EGFR or its activating mutant T790M, treated with inhibitors for 24 hr and analyzed for activating phosphorylation (p) by immunoblot. Actin and total levels of expressed kinases serve as loading controls. Cells transfected with empty plasmid serve as transfection control. (D) Evidence demonstrating that 2 and 5 μM nilotinib inhibits expression of transfected FGFR2, MET and RON. (E) Inhibition of LTK and INSR autophosphorylation by nilotinib. (B–E) Data show a representative experiment for three independent experiments.

2017

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Figure 1—figure supplement 2. Conservation of phosphoepitopes in the intracellelular domains of ALK and LTK. ; (A) Schematic overview of anaplastic lymphoma kinase (ALK) and leukocyte tyrosine kinase (LTK) protein domain structure. (B) Alignment of the intracellular region of ALK and LTK, highlighting in yellow the Y1278 phosphoepitope in the activation loop which shares significant homology between ALK and LTK, and the Y1604 phosphoepitope of ALK which is not found in LTK.

2015

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Figure 4—figure supplement 3. ALK and LTK interact in the presence of FAM150A. FAM150A and anaplastic lymphoma kinase (ALK) coimmunoprecipitate with leukocyte tyrosine kinase (LTK). ; Immunoprecipitation with either anti-IgG control or anti-HA (LTK) was performed and the resulting immonoprecipitates immunoblotted for the presence of ALK (mAb135), LTK (HA) and FAM150A. *indicates immunoglobulin light and heavy chains.

2015

unknown

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Detailansicht für Treffer 5 öffnen

Figure 4—figure supplement 1. FAM150A binds to the extracellular domain of human ALK by ELISA. ; Purified FAM150A was coated on plates and binding of extracellular domain of ALK (ALK-ECD-Fc) was detected by anti-Fc HRP conjugate. LTK-ECD-Fc was used as a binding positive control. FAM150A binds specifically to the ECD of human ALK.

2015

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