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Curr Clin Microbiol Rep. 2014 Dec 1;1(3-4):37-50.

Isoprenoid metabolism in apicomplexan parasites.

Author information

1
Department of Molecular Microbiology Washington University School of Medicine St. Louis, MO 63110 USA limlay@wustl.edu.
2
Department of Pediatrics Washington University School of Medicine St. Louis, MO 63110 USA & Department of Molecular Microbiology Washington University School of Medicine St. Louis, MO 63110 USA.

Abstract

Apicomplexan parasites include some of the most prevalent and deadly human pathogens. Novel antiparasitic drugs are urgently needed. Synthesis and metabolism of isoprenoids may present multiple targets for therapeutic intervention. The apicoplast-localized methylerythritol phosphate (MEP) pathway for isoprenoid precursor biosynthesis is distinct from the mevalonate (MVA) pathway used by the mammalian host, and this pathway is apparently essential in most Apicomplexa. In this review, we discuss the current field of research on production and metabolic fates of isoprenoids in apicomplexan parasites, including the acquisition of host isoprenoid precursors and downstream products. We describe recent work identifying the first MEP pathway regulator in apicomplexan parasites, and introduce several promising areas for ongoing research into this well-validated antiparasitic target.

KEYWORDS:

Apicomplexa; Plasmodium; fosmidomycin; isoprenoid; metabolism; methylerythritol phosphate (MEP) pathway

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