Fig. 6: Acetylation promotes the stability of ACSL4.

A HAT1 or B SIRT3 was knocked down in NPC cells, and the protein expression of ACSL4 was detected by western blot after CHX (10 μg/mL) treatment for different times (0, 4, 8, 12, 24 h). C HAT1 was knocked down and D SIRT3 was knocked down or overexpressed in NPC cells, the protein expression of ACSL4 was detected by western blot after treated with MG-132 (20 μM) for 24 h. E After knockdown of HAT1 and F overexpression of SIRT3 in NPC cells and treated with MG-132 (20 μM) for 10 h, the ubiquitination of ACSL4 was detected by IP assay. G ACSL4 acetylation site by mass spectrometry. After ACSL4-WT, ACSL4-K383R and ACSL4-K383Q plasmids were transfected into 293 T cells, H the acetylation of ACSL4 was detected by IP assay. I Treated with CHX (10 μg/mL) for different time (0, 4, 8, 12, 24 h), the protein expression of ACSL4 was detected by western blot. J, K Indicated plasmids were transfected into 293 T cells, then treated with MG-132 (20 μM) for 10 h, the ubiquitination of ACSL4 was detected by IP assay. Negative control (NC). Blank plasmid (vec).