Fig. 8. Hypothetical signaling pathway inhibiting ecdysteroidogenesis in the crustacean Y-organ. Molt inhibiting hormone (MIH) binds to a G protein-coupled receptor (G), activating adenylyl cyclase (AC); intracellular Ca²⁺ rises when protein kinase A (PKA) activates a membrane Ca²⁺ channel; nitric oxide synthase (NOS) is activated and released from the membrane when Ca²⁺/calmodulin (CaM) binds, and NOS is dephosphorylated by the Ca²⁺/calmodulin-dependent phosphatase, calcineurin (CaN); NO activates an NO-sensitive (class I) GC (GC-I). Activation of a cGMP-dependent protein kinase (cGPK) inhibits expression and/or activities of ecdysteroidogenic proteins, resulting in reduced ecdysteroid synthesis. NOS is inactivated by phosphorylation by PKA, protein kinase C (PKC) or other protein kinases.