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. 2019 Jan 22;68(4):747–760. doi: 10.2337/db18-0671

Figure 2.

Figure 2

GRP94 KD or KO does not lead to β-cell death and induces ER stress via the PERK-ATF4-CHOP pathway. A: SDS-PAGE and WB analysis of GRP94 expression levels in INS-1E cells after lentiviral transduction with GRP94 targeting shRNA (cells lysed 2 weeks after viral transduction, KD) or CRISPR/Cas9 guide GRP94-directed RNA (clonal cell line shown 3 months after viral transduction, KO); n = 5. B: Apoptosis levels (representing internucleosomal degradation of genomic DNA) were analyzed in GRP94 KD and KO (clone 1 and 2) and control cells exposed for 24 h to 1 μmol/L of thapsigargin (Tg); n = 4. C: mRNA levels of ER stress pathways and Ins-1/2 genes were analyzed by quantitative RT-PCR in INS-1E control and GRP94 KD cells. The Ire1 inhibitor 4q8C (Ire1i) was used at 30 μmol/L for 4 h. Data represent the means ± SD analyzed by Bonferroni-corrected paired Student t test of treatments vs. control, *P < 0.02; ***P < 0.0005; n = 6. Ctrl, control.