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. 2017 Jul 21;3:20. doi: 10.1186/s40780-017-0090-y

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — The proposed pathway via which TJ24 and TJ68 promote phosphorylation and support NGF-induced neurite outgrowth. TJ24 and TJ68 promoted neurite outgrowth by activating phosphorylation of both the Erk1/2 and Akt pathways, which in turn supports the function of NGF in extending neurites in cases of paclitaxel-induced neuropathy. NGF: nerve growth factor; Erk 1/2: extracellular signal-related kinase 1/2