Fig. 8: AF1q protects N-Myc from degradation by modulating AKT/GSK3β and Ras/ERK signaling.
From: AF1q is a universal marker of neuroblastoma that sustains N-Myc expression and drives tumorigenesis
A Immunoblot showing reduced levels of N-Myc, phospho-ERK (ERKP, active form) and phospho-GSK3β (GSK3βP, inactive form) but no effect on total ERK (ERKT) or total GSK3β (GSK3βΤ) in Lan-5 cells depleted of AF1q compared to control. GAPDH is a loading control. B Similar results for AF1q silenced and control Kelly cells. C Immunoblot showing reduced levels of phospho-AKT (AKTP, active form) but no effect on total AKT (AKTT) in Lan-5 and Kelly cells treated with AF1q knockdown compared to corresponding controls. D Immunoblot showing expression of Ras, AF1q and phosphorylated ERK (ERKP, active form) in Lan-5 cells transduced with either oncogenic Ras alone or in combination with AF1q knockdown (AF1q KD). Actin and GAPDH are loading controls. Lan-5 cells were harvested 96 h and Kelly cells 120 h post transduction with shAF1q.
