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Fig. 4 | Molecular Autism

Fig. 4

From: TSC patient-derived isogenic neural progenitor cells reveal altered early neurodevelopmental phenotypes and rapamycin-induced MNK-eIF4E signaling

Fig. 4

Rapamycin induced activation of eIF4E and ERK1/2 is partly dependent on PI3K activation. a Treatment with wortmannin (500 nM or 1 μM for 3 h) combined with rapamycin (100 nM for 24 h) in TSC1-Null NPCs decreases phosphorylation of eIF4E; n = 3. b Treatment with wortmannin (1 μM for 3 h) alone or in combination with rapamycin (100 nM for 24 h) inhibits pAKT (s473) and decreases phosphorylation of ERK1/2 in TSC1 mutant NPCs; n = 3. pS6 serves as a control. For each panel, protein expression was quantified and normalized to the Corr-WT NPCs treated with DMSO. Mean values ± S.D. of three separate experiments are shown, *p < 0.01, **p < 0.001 calculated with Student’s t test

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Molecular Autism

ISSN: 2040-2392