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. 2021 Jan 21;19:8. doi: 10.1186/s12964-020-00696-6

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 7 — Working model of Slit/Robo feedback regulation of testosterone synthesis. LH interacts with its membrane receptor, LHCGR (1), to promote the phosphorylation of the transcription factor CREB by PKA and (potentially) AKT (2, 3). This leads to the activation of the transcription of steroidogenic genes and testosterone synthesis (4). Testosterone then enhances the expression of Slit and Robo genes (5, 6) to decrease Leydig cell steroidogenic activity by antagonizing LH signaling. This is potentially achieved both by decreasing AKT-induced CREB phosphorylation (7) and by decreasing Lhcgr expression (8)