Fig. 4
From: Mutant α-synuclein causes death of human cortical neurons via ERK1/2 and JNK activation
PD patient-derived cortical neurons show higher levels of phosphorylated ERK1/2 and JNK. A, B Western blots and quantification data of differentiated cortical neurons for phosphorylated ERK1/2 (p-ERK1/2), ERK1/2 and β-actin (ACTB) on day 8 after neuronal induction. Phosphorylated ERK1/2 levels were normalized by ERK1/2 levels (n = 3 biological replicates; two-tailed Student’s t-test; *p < 0.05). C, D Western blots and quantification data of differentiated cortical neurons for phosphorylated JNK (p-JNK), JNK and β-actin (ACTB) on day 8 after neuronal induction. Phosphorylated JNK levels were normalized by JNK levels (n = 3 biological replicates; two-tailed Student’s t-test; *p < 0.05). E, F Western blots and quantification data of differentiated cortical neurons for phosphorylated p38 (p-p38), p38 and β-actin (ACTB) on day 8 after neuronal induction. Phosphorylated p38 levels were normalized by p38 levels (n = 3 biological replicates; two-tailed Student’s t-test; N.S. not significant). Bar graphs represent mean ± SD