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Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry
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InsP3 Signaling in Apicomplexan Parasites.

Celia R S Garcia1, Eduardo Alves2, Pedro H S Pereira1,2

  • 1Departamento de Fisiologia, Instituto de Biociências, Universidade de São Paulo. Sao Paulo 05508-090, Brazil

Current Topics in Medicinal Chemistry
|February 1, 2017
PubMed
Summary

Apicomplexan parasites produce myo-inositol 1,4,5-trisphosphate (InsP3) for calcium signaling, yet lack identified InsP3 receptors (InsP3Rs). This suggests a potential primitive or non-canonical InsP3R, offering therapeutic targets.

Keywords:
Apicomplexan parasitesCalcium signalingInsP3 signalingPhosphoinositidesPlasmodium

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Area of Science:

  • Cellular Biology
  • Parasitology
  • Biochemistry

Background:

  • Phosphoinositides (PIs) are vital cell membrane components regulating cellular functions.
  • Myo-inositol 1,4,5-trisphosphate (InsP3) generation via phospholipase C (PLC) hydrolysis of PIP2 initiates calcium signaling.
  • InsP3 acts as a second messenger, triggering intracellular calcium release from the endoplasmic reticulum by binding to InsP3 receptors (InsP3Rs).

Purpose of the Study:

  • Investigate the presence and nature of InsP3 receptors in Apicomplexa.
  • Explore the implications of InsP3 signaling in apicomplexan parasites for understanding early eukaryotic evolution.
  • Identify potential therapeutic targets within apicomplexan InsP3 signaling pathways.

Main Methods:

  • Genomic analysis to identify potential InsP3R homologs in apicomplexan species.
  • Biochemical assays to study InsP3 production and its role in calcium signaling.
  • Comparative analysis of PI signaling pathways across different eukaryotic lineages.

Main Results:

  • Apicomplexan genomes lack canonical InsP3Rs despite evidence of InsP3 production.
  • Evidence suggests apicomplexans may possess a primitive or non-canonical InsP3R.
  • InsP3 signaling pathways in apicomplexans diverge from those in animal systems.

Conclusions:

  • The absence of canonical InsP3Rs in apicomplexans points to unique signaling mechanisms.
  • Understanding these non-canonical pathways can illuminate early eukaryotic signaling evolution.
  • Targeting apicomplexan InsP3 signaling pathways presents a promising avenue for novel therapeutic interventions against parasitic infections.