Figure S5.

PERK boosts the OCR independently of its ER stress activity but through E-Syt1 interaction. (A) Representative images showing the transfection efficiency (shown as merge of mCherry and BF channel) in WT and DKO HeLa cells transfected with mCherry empty vector (EV), DKO with mCherry-E-Syt1- ΔSMP and used in Fig. 5, E and F. Scale bar, 100 µm. (B) Representative images showing the transfection efficiency (shown as merge of mCherry and BF channel) in WT and DKO HeLa cells transfected with mCherry empty vector (EV), DKO with mCherry-E-Syt1, or mCherry-E-Syt1- ΔCDE and used in Fig. 5, C and D. Scale bar, 100 µm. (C) Representative immunoblot for E-Syt1 and GFP in WT HeLa cells electroporated with eGFP and DKO HeLa cells electroporated with eGFP, eGFP-E-Syt1, eGFP-E-Syt1-ΔSMP, eGFP-E-Syt1-ΔDE and used in Fig. 6, F and G. Arrows indicate GFP signals for eGFP-empty vector and eGFP-E-Syt1 mutants transfected and E-Syt1 signals for E-Syt1 endogenous and eGFP-E-Syt1 mutants transfected. (D) Quantification of E-Syt1 expression levels normalized on ACTIN (loading control) in WT, DKO + GFP-E-Syt1 full length, DKO + GFP-E-Syt1-ΔSMP, and DKO + GFP-E-Syt1-ΔDE HeLa cells. The values plotted are the mean ± SEM from three biological replicates analyzed using one-way ANOVA, with Tukey’s test for multiple comparisons. NS = not significant. Source data are available for this figure: SourceData FS5.

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