Fig. 7
From: Slit/Robo signaling regulates Leydig cell steroidogenesis
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)