Anion channels in Plasmodium-falciparum-infected erythrocytes and protein kinase A.
By replicating within red blood cells, malaria parasites are largely hidden from immune recognition; however, in the cells, nutrients are limiting and hazardous metabolic end products can rapidly accumulate. Therefore, to survive within erythrocytes, parasites alter the permeability of the host plasma membrane, either by upregulating existing transporters or by creating new permeation pathways. Recent electrophysiological studies of Plasmodium-infected erythrocytes have demonstrated that membrane permeability is mediated by transmembrane transport through ion channels in the infected erythrocyte. This article discusses the evidence and controversies concerning the nature of these channels and surveys the potential role of phosphorylation in activating anion channels that could be important in developing novel strategies for future malarial chemotherapies.
Merckx
Anaïs
A
Institut Cochin, INSERM U567, Université Paris Descartes, CNRS (UMR 8104), Paris, France.
Bouyer
Guillaume
G
Thomas
Serge L Y
SL
Langsley
Gordon
G
Egée
Stéphane
S
D000818:Animals; D000838:Anions; D002463:Cell Membrane Permeability; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology*; D005786:Gene Expression Regulation; D006790:Host-Parasite Interactions; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D016778:Malaria, Falciparum / Q000469:parasitology; D010963:Plasmodium falciparum / Q000201:enzymology / Q000472:pathogenicity / Q000502:physiology*
D000838:Anions; D007473:Ion Channels; D017868:Cyclic AMP-Dependent Protein Kinases