Fig. 4: USP25 maintains the stability of KEAP1.
a Western blotting analysis of KEAP1 in USP25-depleted and control HepG2 cells treated with and without the proteasome inhibitor MG132 (20 μM) for 6 h (n = 3 biologically independent experiments). b Western blotting analysis of KEAP1 in HepG2 cells transfected with GFP-, WT USP25-, or USP25C178S-expressing plasmids (n = 3 biologically independent experiments). c Measurement of the half-lives of KEAP1 in HepG2 cells depleted of USP25 expression through cycloheximide chasing (n = 2 biologically independent experiments). d Measurement of the half-lives of KEAP1 in HepG2 cells transfected with GFP-, WT USP25-, or USP25C178S-expressing plasmids through cycloheximide chasing (n = 2 biologically independent experiments). e Western blotting analysis of the ubiquitinated species of endogenous KEAP1 in HepG2 cells depleted of USP25. The cells were treated with MG132 (20 μM) for 6 h before harvesting for analysis (n = 2 biologically independent experiments). f Western blotting analysis of the ubiquitinated species of endogenous KEAP1 in HepG2 cells transfected with GFP-, WT USP25-, or USP25C178S-expressing plasmids. The cells were treated with MG132 (20 μM) for 6 h before harvesting for analysis (n = 2 biologically independent experiments). Source data are provided as a Source Data file.
