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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Mol Biochem Parasitol. 2009 Jan 21;165(1):1–7. doi: 10.1016/j.molbiopara.2009.01.003

Fig. 1.

Fig. 1

Schematic pathway of signaling in Plasmodium. AC adenylate cyclase, camK calcium/calmodulin kinase B, PDE phosphodiesterase, PLC phospholipase C, PKA protein kinase A, PKG protein kinase G PV parasitophorous vacuole, N nuclei, SR serpentine receptor. Tryptophan-derivatives are able to increase citoplasmic calcium through PLC. Calcium increase activates adenylate cyclase that convert AMP in cAMP once the concentration of such molecule is augmented in response to calcium increase by melatonin. cAMP is able to bind the regulatory subunit of PKA (cyclic AMP-dependent protein kinase) leading to an allosteric change in conformation which causes unleashing of the catalytic subunits becoming it activated and able to phosphorylate its targets. The molecular downstream effects of calcium and PKA in this pathway are proposed.