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. Author manuscript; available in PMC: 2013 Aug 2.
Published in final edited form as: J Am Coll Cardiol. 2011 Jun 21;57(25):2527–2538. doi: 10.1016/j.jacc.2011.02.037

Figure 6. Blunting of Mitogenic and Chemotactic Signaling by a Combination Mutant That Lacks the PI3K and PLCγ Binding Sites (F3 Receptor).

Figure 6

(A) Schematic diagram illustrating the cytoplasmic domain of the chimeric receptor (ChiR)-F3 mutant harboring Tyr-to-Phe substitutions at tyrosine residues 740/51 and 1021. (B) Expression levels of ChiR-F3 in comparison with ChiR-wild type (WT)–expressing cells. (C) Binding characteristics of platelet-derived growth factor beta receptor–associated signaling molecules in quiescent and macrophage colony-stimulating factor (M-CSF)–stimulated ChiR-WT and ChiR-F3 expressing cells. (D, E) M-CSF–dependent chemotaxis and cell cycle progression in WT and ChiR-F3 expressing vascular smooth muscle cells (VSMCs). (F) Effect of M-CSF on cyclin D1 and p27kip1 levels in ChiR-F3 expressing VSMCs. Data in D and E represent mean ± SEM from 3 independent experiments (*p < 0.05 vs. WT). BrdU = 5-bromodeoxyuridine; CSF1R = colony-stimulating factor-1 receptor; other abbreviations as in Figure 1.