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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.





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