کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5916081 | 1163364 | 2007 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Plasmodium falciparum Na+/H+ exchanger activity and quinine resistance
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کلمات کلیدی
NMDGPfMDR1PfCRTsDCMP. falciparumamodiaquineNHEQnrCQRBCECF-AMChrPGPCCCPEIPALSCMQTLSCP2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl esteriRBCROIMDRPlasmodium falciparum chloroquine resistance transporterBSA - BSAP-glycoprotein - P-گلیکوپروتئینbovine serum albumin - آلبومین سرم گاوQuantitative trait loci - تعداد صفات صفاتMalaria - مالاریاMultidrug resistance - مقاومت چند داروییmefloquine - ملفوخینregion of interest - منطقه مورد نظرLaser scanning confocal microscopy - میکروسکوپ کانوکنال اسکن لیزرdigestive vacuole - واکسن گوارشیCarbonyl cyanide 3-chlorophenylhydrazone - کربنیل سیانید 3-کلروفنیل هیدرازونChromosome - کروموزمChloroquine - کلروکین Quinine - کوینینQuinidine - کینیدینinfected red blood cell - گلبول قرمز آلوده
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Mutations in the Plasmodium falciparum pfcrt gene cause resistance to the 4-amino quinoline chloroquine (CQ) and other antimalarial drugs. Mutations and/or overexpression of a P. falciparum multidrug resistance gene homologue (pfmdr1) may further modify or tailor the degree of quinoline drug resistance. Recently [Ferdig MT, Cooper RA, Mu JB, et al. Dissecting the loci of low-level quinine resistance in malaria parasites. Mol Microbiol 2004;52:985-97] QTL analysis further implicated a region of P. falciparum chromosome 13 as a partner (with pfcrt) in conferring resistance to the first quinoline-based antimalarial drug, quinine (QN). Since QN resistance (QNR) and CQR are often (but not always) observed together in parasite strains, since elevated cytosolic pH is frequently (but not always) found in CQR parasites, and since the chr 13 segment linked to QNR prominently harbors a gene encoding what appears to be a P. falciparum Na+/H+ exchanger (PfNHE), we have systematically measured cytosolic pH and PfNHE activity for an extended series of parasite strains used in the QTL analysis. Altered PfNHE activity does not correlate with CQR as previously proposed, but significantly elevated PfNHE activity is found for strains with high levels of QNR, regardless their CQR status. We propose that either an elevated pHcyt or a higher vacuolar pH-to-cytosolic pH gradient contributes to one common route to malarial QNR that is also characterized by recently defined chr 13-chr 9 pairwise interactions. Based on sequence analysis we propose a model whereby observed polymorphisms in PfNHE may lead to altered Na+/H+ set point regulation in QNR parasites.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Biochemical Parasitology - Volume 153, Issue 1, May 2007, Pages 48-58
Journal: Molecular and Biochemical Parasitology - Volume 153, Issue 1, May 2007, Pages 48-58
نویسندگان
Tyler N. Bennett, Jigar Patel, Michael T. Ferdig, Paul D. Roepe,