InsP3 Signaling in Apicomplexan Parasites

Title:InsP3 Signaling in Apicomplexan Parasites

Volume: 17 Issue: 19

Author(s): Celia R.S. Garcia*, Eduardo Alves, Pedro H. S. Pereira, Paula J. Bartlett, Andrew P. Thomas, Katsuhiko Mikoshiba, Helmut Plattner and L. David Sibley

Affiliation:

• Departamento de Fisiologia, Instituto de Biociências, Universidade de São Paulo. Sao Paulo 05508-090,Brazil

Keywords: Calcium signaling, InsP3 signaling, Apicomplexan parasites, Phosphoinositides, Plasmodium.

Abstract: Background: Phosphoinositides (PIs) and their derivatives are essential cellular components that form the building blocks for cell membranes and regulate numerous cell functions. Specifically, the ability to generate myo-inositol 1,4,5-trisphosphate (InsP3) via phospholipase C (PLC) dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) to InsP3 and diacylglycerol (DAG) initiates intracellular calcium signaling events representing a fundamental signaling mechanism dependent on PIs. InsP3 produced by PI turnover as a second messenger causes intracellular calcium release, especially from endoplasmic reticulum, by binding to the InsP3 receptor (InsP3R). Various PIs and the enzymes, such as phosphatidylinositol synthase and phosphatidylinositol 4-kinase, necessary for their turnover have been characterized in Apicomplexa, a large phylum of mostly commensal organisms that also includes several clinically relevant parasites. However, InsP3Rs have not been identified in genomes of apicomplexans, despite evidence that these parasites produce InsP3 that mediates intracellular Ca2+ signaling.

Cite this article as:

Garcia R.S. Celia*, Alves Eduardo, Pereira H. S. Pedro, Bartlett J. Paula, Thomas P. Andrew, Mikoshiba Katsuhiko, Plattner Helmut and Sibley David L., InsP3 Signaling in Apicomplexan Parasites, Current Topics in Medicinal Chemistry 2017; 17 (19) . https://dx.doi.org/10.2174/1568026617666170130121042