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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: N822K- or V560G-mutated KIT activation preferentially occurs in lipid rafts of the Golgi apparatus in leukemia cells

Fig. 2

KIT mutants localize to EL but not to the PM in leukemia cells. a & b Kasumi-1 (a) or HMC-1.1 cells (b) were double-stained with anti-KIT (green) plus the indicated antibody (red). Insets show magnified images. Bars, 10 μm. c Pearson’s R correlation coefficients were calculated by analyzing the intensity of KIT vs. organelle markers. Results are means ± s.d. (n = 12~22). *P < 0.05, ***P < 0.001. NS, not significant. Calnexin (ER marker); giantin (Golgi marker); GM130 (Golgi marker); TFR (endosome marker); LAMP1 (lysosome marker); cathepsin D (cathD, lysosome marker). d Lysates from Kasumi-1 (left) or HMC-1.1 cells (right) were treated with peptide N-glycosidase F (PNGase F) or endoglycosidase H (endo H) then immunoblotted with anti-KIT. CG, complex-glycosylated form; HM, high mannose form; DG, deglycosylated form. Note that most KIT was present in a complex-glycosylated form in these leukemia cells

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