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. 2023 May 16;14:2241. doi: 10.1038/s41467-023-37714-3

Fig. 6. ICG prevents cells from AMA-induced cell death by inhibiting STT3B activity.

Fig. 6

a Intracellular co-localization of ICG and ER in HAP1 and HepG2 cells and the corresponding fluorescence intensity profiles across the cell along the direction of arrow. b A scheme of ER-LucT reporter system, the disruption of luciferase glycosylation turn on luminescence. Luc, luciferase. c N-glycosylation of Luc reduced the Luc activity in HAP1 cells (n = 3 biological replicates). **p = 0.0012 d The blockage of N-glycosylation of Luc increased the Luc activity by treatment with 10 μM ICG. The ER-LucT-activity was normalized to the vehicle control (n = 3 biological replicates). ****p < 0.0001. e N-glycosylation of Luc reduced the Luc activity in HAP1 cells (n = 3 biological replicates). ****p < 0.0001. f The blockage of N-glycosylation of Luc increased the Luc activity by treatment with 100 μM ICG HepG2. The ER-LucT-activity was normalized to the vehicle control (n = 3 biological replicates). ***p = 0.0001. Data are presented as mean ± SD and are representative of three independent experiments. The statistics were all assessed using two-tailed unpaired t test. Source data are provided as a Source Data file.