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View full-text article in PMC

. 2019 Aug 22;8(9):956. doi: 10.3390/cells8090956

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Signalling through the mTORC1, GSK3β, and pathways related to proteins synthesis and axon regeneration. Neurotrophins (NT) act on tyrosine kinase (Trk) receptors and induce phosphatidylinositol kinase (PI3K) activity, which converts phosphatidylinositol (4,5) bisphosphate (PIP2) to phosphatidylinositol (3,4,5) triphosphate (PIP3). Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) catalyses the reverse reaction. PIP3 activates phosphatidylinositol-dependent protein kinase 1 (PDK1), Akt phosphorylation, and inhibits tuberous sclerosis complex (TSC1/2). TSC1/2 can stimulate the Ras homolog enriched in the brain (Rheb) to upregulate mTOR activity. Akt can also inhibit GSK3β, which in turn disinhibits CREB-mediated NT transcription, APC, and CRMP2 to promote growth cone assembly.