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Fig. 6 | Molecular Autism

Fig. 6

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

Fig. 6

Model depicting downstream signaling pathways in untreated and rapamycin-treated TSC1-mutant NPCs. a In untreated TSC1-mutant NPCs, loss of the TSC protein complex results in activated MEK-ERK and mTORC1 signaling. Activated mTORC1 leads to phosphorylation and release of the inhibitory 4EBP1 from the eIF4E subunit enabling the formation of an active eIF4F complex. b Upon rapamycin (Rapa) treatment, while mTORC1-dependent eIF4E activation is inhibited, an alternate mechanism of MNK-mediated eIF4F phosphorylation/activation is enhanced, which is blocked by co-treatment with the MNK inhibitor eFT508

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Molecular Autism

ISSN: 2040-2392