ArticleProceedings of the National Academy of Sciences of the United States of America2007
Toward a unifying model of malaria-induced channel activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Across species: A comparative perspective on red cell homeostasis and its influence on our understanding of human physiology and disease.British journal of haematology · 2026Review
- Hydroxychloroquine's diverse targets: a new frontier in precision medicine.Frontiers in immunology · 2025Review
- The Chloride Conductance Inhibitor NS3623 Enhances the Activity of a Non-selective Cation Channel in Hyperpolarizing Conditions.Frontiers in physiology · 2021Article
- Channelizing the red blood cell: molecular biology competes with patch-clamp.Frontiers in molecular biosciences · 2015Article
- 1,4-naphthoquinones and other NADPH-dependent glutathione reductase-catalyzed redox cyclers as antimalarial agents.Current pharmaceutical design · 2013Review
- X-ray microanalysis investigation of the changes in Na, K, and hemoglobin concentration in plasmodium falciparum-infected red blood cells.Biophysical journal · 2011Article
- Local membrane deformations activate Ca2+-dependent K+ and anionic currents in intact human red blood cells.PloS one · 2010Article
- Malaria parasite mutants with altered erythrocyte permeability: a new drug resistance mechanism and important molecular tool.Future microbiology · 2010Review
- Complex inheritance of the plasmodial surface anion channel in a Plasmodium falciparum genetic cross.Molecular microbiology · 2009Article
- The homeostasis of Plasmodium falciparum-infected red blood cells.PLoS computational biology · 2009Article
- The Plasmodium falciparum-induced anion channel of human erythrocytes is an ATP-release pathway.Pflugers Archiv : European journal of physiology · 2009Article
- Plasmodium falciparum regulatory subunit of cAMP-dependent PKA and anion channel conductance.PLoS pathogens · 2008Article
- ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.Tissue barriersReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of RBC by the malaria parasite Plasmodium falciparum activates, at the trophozoite stage, a membrane current 100- to 150-fold larger than in uninfected RBC. This current is carried by small anion channels initially described in supraphysiological ion concentrations (1.115 M Cl(-)) and named plasmodial surface anion channels (PSAC), suggesting their plasmodial origin. Our results obtained with physiological ion concentrations (0.145 M Cl(-)) support the notion that the parasite-induced channels represent enhanced activity versions of anion channels already present in uninfected RBCs. Among them, an 18-pS inwardly rectifying anion channel (IRC) and a 4- to 5-pS small conductance anion channel (SCC) were present in most single-channel recordings of infected membranes. The aim of this study was to clarify disparities in the reported electrophysiological data and to investigate possible technical reasons why these discrepancies have arisen. We demonstrate that PSAC is the supraphysiological correlate of the SCC and is inhibited by Zn(2+), suggesting that it is a ClC-2 channel. We show that in physiological solutions 80% of the membrane conductance in infected cells can be accounted for by IRC and 20% can be accounted for by SCC whereas in supraphysiological conditions the membrane conductance is almost exclusively carried by SCC (PSAC) because the IRC is functionally turned off.
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