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. 2015 May 18;29(9):3702–3712. doi: 10.1096/fj.15-270645

Figure 1.

Figure 1.

EGF-dependent activation of ERK and AKT survival signaling is abolished in PS1-deficient neurons. A) PCNC from WT (+/+), PS1 heterozygous (+/−), and PS1 homozygous (−/−) KO embryonic mouse brains cultured in 6-well plates were treated at 9 DIV with 20 ng/ml EGF or Hb-EGF for 15 min. After incubation, lysates were collected and probed on WBs for the indicated proteins. B) WT, PS1+/−, or PS1−/− PCNC prepared as above were treated at 9 DIV with 20 ng/ml Hb-EGF. After incubation, lysates were collected at different time points and assayed on WBs for the indicated proteins. Data were obtained from at least 3 separate experiments. C) WT or PS1−/− PCNC as above were treated at 9 DIV with 20 ng/ml Hb-EGF or 100 ng/ml BDNF for 15 min. Nontreated cultures (NT) were used as controls. After incubation, lysates were collected and assayed on WBs for the indicated proteins.