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. 2018 Nov 2;37(22):e99277. doi: 10.15252/embj.201899277

Figure EV1. Lack of cell death, inflammation, and overt ER stress in Sel1L‐deficient hepatocytes.

Figure EV1

  1. TUNEL staining of paraffin‐embedded livers of 9‐week‐old mice with quantitation shown on the right (n = 4 per group, 2 independent repeats).
  2. qPCR analysis of inflammation associated hepatic gene expression in Sel1L f/f and Sel1L Alb mice (n = 4 per group, 3 independent repeats).
  3. Western blot analysis of Sel1L and UPR proteins (Ire1α and BiP) in the livers of 9‐week‐old mice (n = 3 per group, 3 independent repeats). +/− Gly refers to proteins with or without glycosylation; and p/0 refers to phosphorylated or non‐phosphorylated Ire1α. WT mice injected i.p. with tunicamycin (Tm, 1.5 μg/g body weight) for 72 h were included as a control.
  4. RT–PCR analysis of Xbp1 splicing in the livers of 9‐week‐old mice (n = 3 per group, 3 independent repeats); u/s/t refers to unspliced/spliced/total Xbp1. WT mice injected i.p. with tunicamycin (Tm, 1.5 μg/g body weight) for 72 h were included as a control.
  5. RT–PCR analysis of Xbp1 splicing in primary mouse hepatocytes (n = 2 per group, 2 independent repeats). WT primary hepatocytes treated with 200 nM thapsigargin (Tg) for 6 h were included as a control. Quantitation of the percent of Xbp1s in total Xbp1 mRNA is shown below.
Data information: Hsp90, loading control for Western blot analysis. Ribosomal L32, loading control for qPCR and RT–PCR analysis. Values are mean ± SEM; *P < 0.05; **P < 0.01; n.s., not significant by Student's t‐test.