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With the emergence of artemisinin resistance, the efficacy of the partner drugs in the artemisinin combination therapies (<jats:styled-content style=\"fixed-case\">ACT<\/jats:styled-content>) that include quinoline\u2010based drugs is becoming critical. So far only few resistance markers have been identified from which only two transmembrane transporters namely <jats:styled-content style=\"fixed-case\">PfMDR<\/jats:styled-content>1 (an <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\u2010binding cassette transporter) and <jats:styled-content style=\"fixed-case\">PfCRT<\/jats:styled-content> (a drug\u2010metabolite transporter) have been experimentally verified. Another <jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><\/jats:styled-content><jats:italic>.\u2009falciparum<\/jats:italic> transporter, the <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\u2010binding cassette containing multidrug resistance\u2010associated protein (<jats:styled-content style=\"fixed-case\">PfMRP2<\/jats:styled-content>) represents an additional possible factor of drug resistance in <jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><\/jats:styled-content><jats:italic>.\u2009falciparum<\/jats:italic>. In this study, we identified a parasite clone that is derived from the <jats:styled-content style=\"fixed-case\">3D7 <jats:italic>P<\/jats:italic><\/jats:styled-content><jats:italic>.\u2009falciparum<\/jats:italic> strain and shows increased resistance to chloroquine, mefloquine and quinine through the trophozoite and schizont stages. We demonstrate that the resistance phenotype is caused by a 4.1\u2009kb deletion in the 5\u2032 upstream region of the <jats:styled-content style=\"fixed-case\"><jats:italic>pfmrp2<\/jats:italic><\/jats:styled-content> gene that leads to an alteration in the <jats:styled-content style=\"fixed-case\"><jats:italic>pfmrp2<\/jats:italic><\/jats:styled-content> transcription and thus increased level of <jats:styled-content style=\"fixed-case\">PfMRP2<\/jats:styled-content> protein. These results also suggest the importance of putative promoter elements in regulation of gene expression during the <jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><\/jats:styled-content><jats:italic>.\u2009falciparum<\/jats:italic> intra\u2010erythrocytic developmental cycle and the potential of genetic polymorphisms within these regions to underlie drug resistance.<\/jats:p>","DOI":"10.1111\/mmi.12505","type":"journal-article","created":{"date-parts":[[2013,12,27]],"date-time":"2013-12-27T04:57:09Z","timestamp":1388120229000},"page":"918-934","source":"Crossref","is-referenced-by-count":31,"title":["Structural polymorphism in the promoter of <scp><i>pfmrp2<\/i><\/scp> confers <scp><i>P<\/i><\/scp><i>lasmodium falciparum<\/i> tolerance to quinoline drugs"],"prefix":"10.1111","volume":"91","author":[{"given":"Sachel","family":"Mok","sequence":"first","affiliation":[{"name":"School of Biological Sciences Nanyang Technological University  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