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1 ion into inert hemozoin within the parasitic digestive vacuole.
2 omineralization within the malarial parasite digestive vacuole.
3 ozoin formation within lipid droplets in the digestive vacuole.
4 ligned hemozoin crystals within the parasite digestive vacuole.
5 lay abnormal ER architecture and an enlarged digestive vacuole.
6 embrane of the intra-erythrocytic parasite's digestive vacuole.
7 mediating the efflux of chloroquine from the digestive vacuole.
8 s is a vast process that occurs in an acidic digestive vacuole.
9  proteolysis of hemoglobin in the Plasmodium digestive vacuole.
10 ake and trafficking of host cytoplasm to the digestive vacuole.
11 d digest abundant host hemoglobin within the digestive vacuole.
12  host erythrocyte hemoglobin in an acidified digestive vacuole.
13 ing starvation, and the formation of central digestive vacuoles.
14 of hemozoin biosynthesis within the parasite digestive vacuoles.
15 stidine-rich protein II (HRP II) in purified digestive vacuoles.
16 te cytosol, HRPs are brought into the acidic digestive vacuole along with hemoglobin.
17 bservation of bromoquine distribution in the digestive vacuole and at its membrane surface, we deduce
18 c and neutral conditions inside a parasite's digestive vacuole and cytosol, respectively.
19  Hemoglobin degradation occurs in the acidic digestive vacuole and is essential for the survival of t
20  to its target ferriprotoporphyrin IX in the digestive vacuole and loss of verapamil reversibility of
21 pmental cycle and is mainly localized to the digestive vacuole and parasite plasma membrane.
22 on of PfA-M1 caused swelling of the parasite digestive vacuole and prevented proteolysis of hemoglobi
23 ations of material were detected in abnormal digestive vacuoles and aggregated at the parasite plasma
24 accumulation of quinolines in the plasmodium digestive vacuole, and suggest that a quinoline heme com
25 ve and -resistant parasites, causes enlarged digestive vacuoles, and renders chloroquine-resistant st
26                          Since intracellular digestive vacuoles are ubiquitously acidified by V-type
27 lobin by sequestering it within the parasite digestive vacuole as a polymer called hemozoin.
28 M17 results in parasites exhibiting multiple digestive vacuoles at the trophozoite stage.
29 ost interior and the parasite's cytoplasm or digestive vacuole (DV) and is only present as a free bas
30 his probe localizes to the malarial parasite digestive vacuole (DV) during initial perfusion under ph
31 embrane-spanning domains and is found in the digestive vacuole (DV) membrane of intraerythrocytic par
32 e proton electrochemical gradient across the digestive vacuole (DV) membrane.
33 (triple-PM KO), and mutants lacking all four digestive vacuole (DV) plasmepsins (pfpm4, pfpm1, pfpm2
34 eporters revealed that PI(3)P stabilizes the digestive vacuole (DV) under heat stress.
35  not only infective merozoites, but also the digestive vacuole (DV), a membrane-bounded organelle con
36  orientation of hemozoin crystals within the digestive vacuole (DV), as a signature of their nucleati
37 nsmembrane protein localizes to the parasite digestive vacuole (DV), the site of CQ action, where inc
38 the volume and pH regulation of the parasite digestive vacuole (DV), using the fluorescence imaging c
39 throcytes by selectively lysing the parasite digestive vacuole (DV).
40 ced rate of ATP-dependent CQ uptake into the digestive vacuole (DV).
41 esent within other compartments, such as the digestive vacuole (DV).
42 moglobin within a specialized organelle, the digestive vacuole (DV).
43  amphipathic glycoside saponin and engenders digestive vacuoles (DVs) that are small and malformed.
44 oglobin into peptides and amino acids in the digestive vacuole for export to the parasite cytoplasm f
45 ficult or impossible with hematin-containing digestive vacuoles from P. falciparum-infected erythrocy
46 inhibit hemozoin formation in the parasite's digestive vacuole in a manner similar to that of chloroq
47  subunits in regulating morphogenesis of the digestive vacuole independent of proton translocation.
48 romultimeric V-ATPase complex to acidify the digestive vacuole matrix, which is essential for intrava
49 ance mechanism operates at the P. falciparum digestive vacuole membrane in malaria.
50 is associated with multiple mutations in the digestive vacuole membrane protein PfCRT.
51 orter (PfCRT), a transporter resident on the digestive vacuole membrane that in its variant forms can
52 esistance transporter, pfcrt, located in the digestive vacuole membrane, confer CQ resistance in Plas
53            This complex is driven toward the digestive vacuole membrane, increasing the chances of me
54 ulated by overexpression or mutations in the digestive vacuole membrane-bound ABC transporter PfMDR1
55 ide polymorphisms in pfmdr1, which encodes a digestive vacuole membrane-bound ATP-binding cassette tr
56 ISPR-Cas9-based gene editing, identified the digestive vacuole membrane-spanning transporter PfMDR1 (
57 functions as a transporter in the parasite's digestive vacuole membrane.
58  4, previously known only to function in the digestive vacuole of asexual blood stage Plasmodium, pla
59 e previously only known to be present in the digestive vacuole of asexual stage malaria parasites.
60                                          The digestive vacuole of Plasmodium falciparum is the site o
61 ation of protonated CQ as a weak base in the digestive vacuole of the erythrocyte-stage parasite, and
62          The maintenance of acidic pH in the digestive vacuole of the malaria parasite is thought to
63 ly that traverses the membrane of the acidic digestive vacuole of the parasite(3-9).
64        Obtaining a definitive measurement of digestive vacuole pH has been surprisingly difficult.
65 tagged dyes as probes for the measurement of digestive vacuole pH has proved problematic, yet some su
66 is associated with an attenuated increase in digestive vacuole pH relative to CVIET pfcrt-carrying is
67  were identified as a novel class of malaria digestive vacuole plasmepsin inhibitors by using NMR-bas
68                                          The digestive vacuole plasmepsins PfPM1, PfPM2, PfPM4, and P
69                       Some, particularly the digestive vacuole plasmepsins, have been extensively cha
70                               Mutations in a digestive vacuole protein encoded by a 13-exon gene, pfc
71 , we find that bromoquine accumulates in the digestive vacuole, reaching submillimolar concentration,
72                            Mutations in both digestive vacuole-resident transporters are thought to d
73  and blockage of hemoglobin digestion in the digestive vacuole, resulting in an arrest of parasite de
74 to efflux chloroquine from the intracellular digestive vacuole, the site of drug action.
75 nthesizes insoluble hemozoin crystals in the digestive vacuole through polymerization of beta-hematin
76 ts peptides from the lumen of the parasite's digestive vacuole to the cytosol, thereby providing a so
77 ered protein localization, from the parasite digestive vacuole to the plasma membrane, of the P. yoel
78 lciparum is associated with mutations in the digestive vacuole transmembrane protein PfCRT.
79 ultiple amino acid mutations in the parasite digestive vacuole transmembrane protein PfCRT.
80  and pfmdr 1, which encode the P. falciparum digestive-vacuole transmembrane proteins PfCRT and Pgh1,
81 oin (Hz) produced within the living parasite digestive vacuole, under physiologic conditions.
82 cumulation of electron-dense vesicles in the digestive vacuole was observed upon disruption of PfPM4;
83 ort, and in association with hemozoin of the digestive vacuole, where chloroquine inhibits heme polym
84 -product of hemoglobin catabolism within the digestive vacuole, where heme is predominantly sequester
85 ffecting multiple processes in the parasitic digestive vacuole, with the possibility of a novel targe