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. 2019 Apr 5;13:128. doi: 10.3389/fncel.2019.00128

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Copyright © 2019 Duraikannu, Krishnan, Chandrasekhar and Zochodne.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Signaling of the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/PI3K/Akt pathway. PTEN converts phosphatidylinositol (3,4,5)-triphosphate (PIP3) into phosphatidylinositol (4,5)-bisphosphate (PIP2), thus inhibiting Akt activation and peripheral nerve regeneration. Activation of PI3K and Akt signals through deletion of PTEN [BPV (pic) or siRNA] increases regeneration of axons in injury. These impacts appear to be independent of mammalian target of rapamycin (mTOR) but require the activity of PI3K and Akt (Duraikannu, original illustration).