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. 2015 Oct 20;6(37):40158–40171. doi: 10.18632/oncotarget.5522

Figure 1. TrkB-mediated c-Src activation induces activation of the PI3K/AKT and Ras-MAPK pathway.

Figure 1

A. Identification of TrkB expression and autophosphorylation in MDA-MB-231 cell lines. Cell extracts were immunoprecipitated using anti-TrkB antibody and Gamma-bind beads, after which they were immunoblotted with anti-phosphotyrosine antibody. B. Western blot analysis of expression of phospho-AKT and cyclin D1 in MDA-MB-231 cells treated with 50 nM K252a or 5 μM SU6656. β-actin was used as a loading control. C. Colony formation assay of MDA-MB-231 cells treated with 5 μM SU6656 (n = 3). *P < 0.001, t-test. D. Western blot analysis of expression of phospho-c-Src and c-Src in MDA-MB-231 control-shRNA or TrkB-shRNA cells. β-actin was used as a loading control. E. Western blot analysis of expression of phospho-AKT, phospho-MEK, and cyclin D1 in MDA-MB-231 control-shRNA or TrkB-shRNA cells. β-actin was used as a loading control. F. Identification of complex formation of endogenous TrkB/c-Src in MBA-MB-231 cells. G. TrkB interacts with the c-Src after transfection with c-Src or TrkB. H. Identification of the c-Src region responsible for TrkB interaction. Immunoblot analysis of whole-cell lysates and immunoprecipitates derived from 293T cells transfected with the V5-TrkB and Myc-c-Src deletion constructs was conducted as indicated. I. Western blot analysis of expression of phospho-c-Src, phospho-AKT, c-Src, AKT, and cyclin D1 in MDA-MB-231 control-shRNA or c-Src-shRNA cells. β-actin was used as a loading control.