Recovery of proteasome activity is DDI2 independent.
a. Expression of DDI2 in the CRISPR-generated clones of HAP1 cells used in this work was analyzed by western blot. The full-size membrane is presented in Fig. S1a. b. The experimental set up in this study. Cells were pulse treated with Btz and Cfz for 1hr, then cultured in a drug-free media, and analyzed at times indicated. c. Wt- and DDI2 KO clones of HAP1 cells were treated for 1hr. The cell viability was measured using CellTiter-Glo, and the inhibition of β5 sites was measured with the Proteasome-Glo assay at times indicated. Data are averages+/-S.E.M. of two to five biological replicates d. Knockout of DDI2 inhibits the Nrf1 processing. Western blots of Btz-treated HAP1 cells. Sample in the first lane are wt cells treated fwith VCP/p97 inhibitor CB-5083, which blocks Nrf1 processing [17-19], immediately after removal of Btz. The full-size membranes and proteasome activity measurements from this experiment are presented in Figs. S1b and S1c. e. MDA-MB-231 and SUM149 cells were analyzed by western blot 72hr after transfection with DDI2 siRNAs. The full-size membranes are presented in Fig. S2. f. The β5 activity in siRNA-transfected SUM149 and MDA-MB-231 treated with 100 nM Btz for 1hr. The β5 activity was measured using Suc-LLVY-AMC immediately and 18 hrs after treatment. Data are averages+/-S.E.M. of three to five biological replicates. Statistical analysis was conducted using mixed-effect multiple comparisons; p-values ≤ 0.05 were considered significant.