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Fig. 3 | BMC Veterinary Research

Fig. 3

From: A canine case of malignant melanoma carrying a KIT c.1725_1733del mutation treated with toceranib: a case report and in vitro analysis

Fig. 3

Analysis of phosphorylation status of KIT and effect of toceranib on the phosphorylation of mutant KIT expressed in human embryonic kidney 293 cells. a Left panel; phosphorylation status of wild-type and mutant KIT in the cells in the presence (+, 100 ng/mL) or absence (−) of canine stem cell factor (SCF) was analyzed by western blotting. pKIT, phosphorylated KIT. Right panel; semiquantitative analysis of the signal levels of pKIT normalized to those of KIT in the left panel is shown. The normalized signal level of pKIT in SCF-stimulated cells expressing mutant KIT was set at 1.0. Data are expressed as the means and standard deviations of three independent experiments. * Statistically significant difference versus non-SCF-stimulated wild-type KIT (P < 0.05, unpaired two-tailed Student’s t test). b Left panel; effect of toceranib (0–1 μM) on the phosphorylation of mutant KIT was analyzed by western blotting. pKIT, phosphorylated KIT. Right panel; semiquantitative analysis of the signal levels of pKIT normalized to those of KIT in the left panel is shown. The normalized signal level of pKIT in the absence of toceranib (0 μM) was set at 1.0. Data are expressed as the means and standard deviations of three independent experiments. * Statistically significant difference versus 0 μM toceranib (P < 0.05, unpaired two-tailed Student’s t test)

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