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. 2015 Nov 16;112(52):15862–15867. doi: 10.1073/pnas.1520099112

Fig. S4.

Fig. S4.

(A–C) Dose-dependent activation of ALK by heparin in NB1, neuroblastoma cells, endogenously expressing ALK. (A) NB1 cells were treated with increasing concentrations of heparin (as indicated) in the presence or absence of 0.064, 0.159, or 1.59 nM of AUG-α (as indicated). (B) NB1 cells were treated with increasing concentrations of heparin (as indicated) in the presence or absence of 0.634 nM, and an inhibitory effect on AUG-α by heparin was observed at high concentrations of heparin. (C) Dose-dependent activation of ALK by heparin in NIH/3T3 cells exogenously expressing ALK. NIH/3T3 cells were treated with increasing concentrations of heparin (as indicated) in the presence or absence of 0.63 nM of AUG-α. No effect by heparin was observed.