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. 2021 Apr 12;12(4):392. doi: 10.1038/s41419-021-03669-w

Fig. 9. Inhibition of Rab7 recruitment to lysosome by CID1067700 aggravated defect of late autophagic flux in NSC34-hSOD1G93A cells.

Fig. 9

AC Simvastatin-treated NSC34-hSOD1G93A cells were incubated with or without GGPP (10 µM) for 24 h, and were treated with GGPP (10 μM) for 24 h combined with CID1067700 (40 μM) for 2 h before cell harvesting. CID1067700, a late endosome GTPase Rab7 receptor antagonist. Nuclei were stained with DAPI (blue). A Immunofluorescence labeling of Rab7 (red) and LAMP2 (green) in per cell group. B Immunofluorescence labeling of LC3 (red) and P62 (green) in per cell group. C Immunofluorescence labeling of LC3 (red) and LAMP2 (green) in the per cell group. (Scale bars, 10 μm). D Schematic view of the potential mechanisms by which simvastatin inhibited Rab7-driven membrane fusion of autophagosomes with lysosomes, leading to aggravated impairment of late autophagic flux and accelerated neuron death.