Plasmodium falciparum and the permeation pathway of the host red blood cell

被引:17
作者
Thomas, SLY
Lew, VL
机构
[1] Univ Cambridge, Physiol Lab, Cambridge CB2 3EG, England
[2] CNRS, Biol Stn, UPR 9042, F-29682 Roscoff, France
基金
英国惠康基金;
关键词
D O I
10.1016/j.pt.2004.01.003
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
invasion of red blood cells by malaria parasites leads to a huge increase in solute traffic across the membrane of a normally tight cell. Recent electrophysiological investigations strongly support earlier evidence from transport and pharmacological studies that the permeability pathway, which the parasite induces in the host cell membrane, is an anion-selective channel. This article analyzes the evidence and controversies concerning the nature of this channel, surveys the main open questions and suggests directions for future research in this area.
引用
收藏
页码:122 / 125
页数:4
相关论文
共 12 条
[1]   A voltage-dependent channel involved in nutrient uptake by red blood cells infected with the malaria parasite [J].
Desai, SA ;
Bezrukov, SM ;
Zimmerberg, J .
NATURE, 2000, 406 (6799) :1001-1005
[2]   A stretch-activated anion channel is up-regulated by the malaria parasite Plasmodium falciparum [J].
Egée, S ;
Lapaix, F ;
Decherf, G ;
Staines, HM ;
Ellory, JC ;
Doerig, C ;
Thomas, SLY .
JOURNAL OF PHYSIOLOGY-LONDON, 2002, 542 (03) :795-801
[3]   Genome sequence of the human malaria parasite Plasmodium falciparum [J].
Gardner, MJ ;
Hall, N ;
Fung, E ;
White, O ;
Berriman, M ;
Hyman, RW ;
Carlton, JM ;
Pain, A ;
Nelson, KE ;
Bowman, S ;
Paulsen, IT ;
James, K ;
Eisen, JA ;
Rutherford, K ;
Salzberg, SL ;
Craig, A ;
Kyes, S ;
Chan, MS ;
Nene, V ;
Shallom, SJ ;
Suh, B ;
Peterson, J ;
Angiuoli, S ;
Pertea, M ;
Allen, J ;
Selengut, J ;
Haft, D ;
Mather, MW ;
Vaidya, AB ;
Martin, DMA ;
Fairlamb, AH ;
Fraunholz, MJ ;
Roos, DS ;
Ralph, SA ;
McFadden, GI ;
Cummings, LM ;
Subramanian, GM ;
Mungall, C ;
Venter, JC ;
Carucci, DJ ;
Hoffman, SL ;
Newbold, C ;
Davis, RW ;
Fraser, CM ;
Barrell, B .
NATURE, 2002, 419 (6906) :498-511
[4]   NEW PERMEABILITY PATHWAYS INDUCED IN MEMBRANES OF PLASMODIUM-FALCIPARUM INFECTED ERYTHROCYTES [J].
GINSBURG, H ;
KRUGLIAK, M ;
EIDELMAN, O ;
CABANTCHIK, ZI .
MOLECULAR AND BIOCHEMICAL PARASITOLOGY, 1983, 8 (02) :177-190
[5]   Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation [J].
Huber, SM ;
Uhlemann, AC ;
Gamper, NL ;
Duranton, C ;
Kremsner, PG ;
Lang, F .
EMBO JOURNAL, 2002, 21 (1-2) :22-30
[6]   Membrane transport in the malaria-infected erythrocyte [J].
Kirk, K .
PHYSIOLOGICAL REVIEWS, 2001, 81 (02) :495-537
[7]   Intraerythrocytic Plasmodium falciparum utilizes only a fraction of the amino acids derived from the digestion of host cell cytosol for the biosynthesis of its proteins [J].
Krugliak, M ;
Zhang, JM ;
Ginsburg, H .
MOLECULAR AND BIOCHEMICAL PARASITOLOGY, 2002, 119 (02) :249-256
[8]   Excess hemoglobin digestion and the osmotic stability of Plasmodium falciparum-infected red blood cells [J].
Lew, VL ;
Tiffert, T ;
Ginsburg, H .
BLOOD, 2003, 101 (10) :4189-4194
[9]   Modulation of whole-cell currents in Plasmodium falciparum-infected human red blood cells by holding potential and serum [J].
Staines, HM ;
Powell, T ;
Ellory, JC ;
Egée, S ;
Lapaix, F ;
Decherf, G ;
Thomas, SLY ;
Duranton, C ;
Lang, F ;
Huber, SM .
JOURNAL OF PHYSIOLOGY-LONDON, 2003, 552 (01) :177-183
[10]   Perturbation of the pump-leak balance for Na+ and K+ in malaria-infected erythrocytes [J].
Staines, HM ;
Ellory, JC ;
Kirk, K .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2001, 280 (06) :C1576-C1587