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. 2018 Oct 26;9(11):1096. doi: 10.1038/s41419-018-1129-1

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Leptin binds to LepRb and activates the PI3K/Akt signaling pathway. Activating LepRb also stimulates the MAPK-signaling pathway. Both pathways promote neuroprotection, cell survival, and proliferation. The stimulation of PI3K/Akt decreases GSK-3β activity by phosphorylating GSK-3, promoting the expression of cell proliferation genes. Activation of the LepRb leads to CREB phosphorylation and initiation of CREB-dependent transcription, which also enhances cell proliferation genes. CREB cAMP response element-binding protein