Skip to main content
Fig. 2 | Molecular Brain

Fig. 2

From: Enhanced primary ciliogenesis via mitochondrial oxidative stress activates AKT to prevent neurotoxicity in HSPA9/mortalin-depleted SH-SY5Y cells

Fig. 2

Loss of IFT88 blocks primary ciliogenesis and ciliary signaling by depleting HSPA9 in SH-SY5Y cells. (A-C) SH-SY5Y cells transiently co-transfected with siHSPA9 with or without IFT88 siRNA (siIFT88) were imaged by staining with ARL13B antibody (green) and Hoechst 33,342 dye (blue) (A). Primary cilia were also observed in the cells under a fluorescent microscope (B). SH-SY5Y cells co-transfected with siHSPA9 with or without siIFT88 were analyzed via western blotting with the indicated antibodies (C). (D) SH-SY5Y cells transiently transfected with scrambled siRNA (Sc) or siHSPA9. After 3 days, the cells were stained with phospho-AKT antibody (green), γ-Tubulin antibody (red), and Hoechst 33,342 dye (blue). Data were obtained from at least three independent experiments and the results are presented as the means ± S.E.M. (n = 3, ** p < 0.01, **** p < 0.001), Scale bar: 5 μm

Back to article page

Molecular Brain

ISSN: 1756-6606