{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T06:46:12Z","timestamp":1787985972963,"version":"build-2784847793"},"reference-count":40,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2005,12,1]],"date-time":"2005-12-01T00:00:00Z","timestamp":1133395200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Eukaryot Cell"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The plasmodial surface anion channel (PSAC), a novel ion channel induced on human erythrocytes infected with\n            <jats:italic>Plasmodium falciparum<\/jats:italic>\n            , mediates increased permeability to nutrients and presumably supports intracellular parasite growth. Isotope flux studies indicate that other malaria parasites also increase the permeability of their host erythrocytes, but the precise mechanisms are unknown. Channels similar to PSAC or alternative mechanisms, such as the upregulation of endogenous host transporters, might fulfill parasite nutrient demands. Here we evaluated these possibilities with rhesus monkey erythrocytes infected with\n            <jats:italic>Plasmodium knowlesi<\/jats:italic>\n            , a parasite phylogenetically distant from\n            <jats:italic>P. falciparum<\/jats:italic>\n            . Tracer flux and osmotic fragility studies revealed dramatically increased permeabilities paralleling changes seen after\n            <jats:italic>P. falciparum<\/jats:italic>\n            infection. Patch-clamp of\n            <jats:italic>P. knowlesi<\/jats:italic>\n            -infected rhesus erythrocytes revealed an anion channel with striking similarities to PSAC: its conductance, voltage-dependent gating, pharmacology, selectivity, and copy number per infected cell were nearly identical. Our findings implicate a family of unusual anion channels highly conserved on erythrocytes infected with various malaria parasites. Together with PSAC's exposed location on the host cell surface and its central role in transport changes after infection, this conservation supports development of antimalarial drugs against the PSAC family.\n          <\/jats:p>","DOI":"10.1128\/ec.4.12.2153-2159.2005","type":"journal-article","created":{"date-parts":[[2005,12,8]],"date-time":"2005-12-08T23:23:25Z","timestamp":1134084205000},"page":"2153-2159","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["The Plasmodial Surface Anion Channel Is Functionally Conserved in Divergent Malaria Parasites"],"prefix":"10.1128","volume":"4","author":[{"given":"Godfrey","family":"Lisk","sequence":"first","affiliation":[{"name":"The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay A.","family":"Desai","sequence":"additional","affiliation":[{"name":"The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.160.5.1585"},{"key":"e_1_3_2_3_2","first-page":"4279","volume":"104","year":"2004","unstructured":"Alkhalil, A., J. V. Cohn, M. A. Wagner, J. S. Cabrera, T. Rajapandi, and S. A. Desai. 2004. Plasmodium falciparum likely encodes the principal anion channel on infected human erythrocytes. Blood104:4279-4286.","journal-title":"Blood"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj2730701"},{"key":"e_1_3_2_5_2","first-page":"3372","volume":"104","year":"2004","unstructured":"Biagini, G. A., E. M. Pasini, R. Hughes, H. P. De Koning, H. J. Vial, P. M. O'Neill, S. A. Ward, and P. G. Bray. 2004. Characterization of the choline carrier of Plasmodium falciparum: a route for the selective delivery of novel antimalarial drugs. 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J. O'Sullivan, and A. M. Gero. 1997. Laboratory and field comparisons of adenosine influx in Plasmodium falciparum and Plasmodium vivax infected erythrocytes with genetic abnormalities from patients in Myanmar. Southeast Asian J. Trop. Med. Public Health28:22-31.","journal-title":"Southeast Asian J. Trop. Med. Public Health"},{"key":"e_1_3_2_28_2","first-page":"113","volume":"152","year":"1948","unstructured":"Overman, R. R. 1948. Reversible cellular permeability alterations in disease. In vivo studies on sodium, potassium and chloride concentrations in erythrocytes of the malarious monkey. Am. J. Physiol.152:113-121.","journal-title":"Am. J. 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