Figure 6. UFM1 and UFBP1 are involved in ER stress induced apoptosis.

INS-1E cells were treated with the ER stressors oleate, palmitate, cyclopiazonic acid (CPA) and brefeldin A or the ER stress-independent apoptosis inducers cycloheximide and H₂O₂, and silenced forUfm1 (A), Ufbp1 (B) or Ufl1 (C). Apoptosis was evaluated by Hoechst/PI staining. Data are means±SEM of 3–7 independent experiments. Paired student t test: *, p≤0.05; **, p≤0.01; ***, p≤0.001 compared to control treatment; #, p≤0.05; ##, p≤0.01 silenced cells compared to siControl cells, D Caspase 3 activation in Ufm1 and Ufbp1 silenced cells after treatment with the ER stressors CPA and brefeldin A (Bref). The densitometric quantification of the immunoblots is shown in the lower panel. Cleaved Caspase-3 signal was normalized for α-tubulin expression. The results are means ± SEM of 2–3 independent experiments. In the assays, the respective controls contain the vehicles ethanol and DMSO.