Skip to main content
. 2017 Feb 1;9(3):371–384. doi: 10.15252/emmm.201606664

Figure EV4. The PERK activator acts via the PERK‐NRF2 pathway.

Figure EV4

  1. Representative Western blot of LUHMES neurons treated with the PERK activator (PA, 200 nM) using an antibody against heme oxygenase‐1 (HO‐1); a GAPDH antibody was used as loading control.
  2. Densitometric analysis of Western blots described in (A) (n = 3), normalized to the loading control and to untreated control cells.
  3. ATP assay of LUHMES neurons either left untreated (control) or transduced with lentiviruses to overexpress mCherry (LV‐mCh), or 4R tau (LV‐4R) and treated without or with the NRF2 activator DL‐sulforaphane N‐acetyl‐L‐cysteine (SFN‐NAC; n = 6 per group) demonstrates that NRF2 activation protects against 4R tau‐induced toxicity.
  4. ATP assay of LUHMES neurons either left untreated (control) or transduced with LV‐mCh or LV‐4R, and with non‐targeting siRNA or siRNA targeting the NRF2 gene NFE2L2 (n = 4 per group), demonstrates that NRF2 downregulation aggravates 4R tau‐induced toxicity. Silencing efficacy of NFE2L2 siRNA was demonstrated by Western blot (Appendix Fig S4).
Data information: Data are mean + SEM. Statistical analysis in (B) was Student's t‐test, in (C, D) two‐way ANOVA followed by Fisher's LSD or Tukey's (D) post hoc test; *P < 0.05, ***P < 0.001.