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. 2017 Aug 7;8(47):82897–82909. doi: 10.18632/oncotarget.19970

Figure 4. Inhibition of KIT D816-mediated signaling pathways by crenolanib.

Figure 4

Isogenic Ba/F3 cells harboring a mutant-KIT D816V isoform (A, left and mid panels), the corresponding mastocytosis cell line HMC1.2 (D816V+, A, right panel), Ba/F3 cells harboring a mutant-KIT D816Y isoform (B, left panel) and the corresponding mastocytosis cell line p815 (murine D814Y, B, right panel) were treated with crenolanib or dasatinib (A) in dose-dilution assays for 90‘. Western immunoblots are shown for inhibition of autophosphorylation of KIT and consecutive downstream signaling via ERK1/2, STAT5 and AKT. Two different phospho-KIT antibodies (monoclonal Tyr703, 145 KDa, polyclonal Tyr719, 120/145 KDa) provide similar results via dephosphorylation of KIT (not degradation as indicated by stable KIT blots) upon crenolanib as well as dasatinib exposure. Tubulin serves as loading control.