Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
about
That Was Then But This Is Now: Malaria Research in the Time of an Eradication AgendaExit of Plasmodium sporozoites from oocysts is an active process that involves the circumsporozoite protein.Falstatin, a cysteine protease inhibitor of Plasmodium falciparum, facilitates erythrocyte invasionPlasmodium falciparum merozoite invasion is inhibited by antibodies that target the PfRh2a and b binding domainsGliding motility of Babesia bovis merozoites visualized by time-lapse video microscopyAn essential malaria protein defines the architecture of blood-stage and transmission-stage parasites.A novel Plasmodium-specific prodomain fold regulates the malaria drug target SUB1 subtilaseA Plasmodium falciparum dipeptidyl aminopeptidase I participates in vacuolar hemoglobin degradationInhibitor of cysteine proteases is critical for motility and infectivity of Plasmodium sporozoitesCalcium-dependent permeabilization of erythrocytes by a perforin-like protein during egress of malaria parasitesHost cell remodeling by pathogens: the exomembrane system in Plasmodium-infected erythrocytesBiochemical properties of a novel cysteine protease of Plasmodium vivax, vivapain-4Biophysics of malarial parasite exit from infected erythrocytesAn EGF-like protein forms a complex with PfRh5 and is required for invasion of human erythrocytes by Plasmodium falciparumA multifunctional serine protease primes the malaria parasite for red blood cell invasionIrreversible effect of cysteine protease inhibitors on the release of malaria parasites from infected erythrocytesMerozoite release from Plasmodium falciparum-infected erythrocytes involves the transfer of DiIC₁₆ from infected cell membrane to Maurer's clefts.Parasitophorous vacuole poration precedes its rupture and rapid host erythrocyte cytoskeleton collapse in Plasmodium falciparum egress.Identification of proteases that regulate erythrocyte rupture by the malaria parasite Plasmodium falciparum.Inhibition of malaria parasite development by a cyclic peptide that targets the vital parasite protein SERA5.The coming-out of malaria gametocytes.The Plasmodium serine-type SERA proteases display distinct expression patterns and non-essential in vivo roles during life cycle progression of the malaria parasite.The malaria parasite progressively dismantles the host erythrocyte cytoskeleton for efficient egressPlasmodium falciparum cysteine protease falcipain-1 is not essential in erythrocytic stage malaria parasites.The role of serine-type serine repeat antigen in Plasmodium yoelii blood stage developmentEnhanced egress of intracellular Eimeria tenella sporozoites by splenic lymphocytes from coccidian-infected chickens.Centenary celebrations article: Cysteine proteases of human malaria parasites.Inhibition of Plasmodium falciparum oocyst production by membrane-permeant cysteine protease inhibitor E64d.Survival of protozoan intracellular parasites in host cells.Plasmodium subtilisin-like protease 1 (SUB1): insights into the active-site structure, specificity and function of a pan-malaria drug target.Apicomplexan parasites co-opt host calpains to facilitate their escape from infected cells.Proteolytic activation of the essential parasitophorous vacuole cysteine protease SERA6 accompanies malaria parasite egress from its host erythrocyte.Localisation-based imaging of malarial antigens during erythrocyte entry reaffirms a role for AMA1 but not MTRAP in invasionDefining the timing of action of antimalarial drugs against Plasmodium falciparum.Changes in the plasmodial surface anion channel reduce leupeptin uptake and can confer drug resistance in Plasmodium falciparum-infected erythrocytes.A host GPCR signaling network required for the cytolysis of infected cells facilitates release of apicomplexan parasites.The M18 aspartyl aminopeptidase of Plasmodium falciparum binds to human erythrocyte spectrin in vitro.Plasmodium falciparum gametocytes: still many secrets of a hidden life.Malarial proteases and host cell egress: an 'emerging' cascade.Expression and processing of Plasmodium berghei SERA3 during liver stages.
P2860
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P2860
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh
2003年學術文章
@zh-hant
name
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@en
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@nl
type
label
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@en
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@nl
prefLabel
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@en
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@nl
P2860
P356
P1476
Selective inhibition of a two-step egress of malaria parasites from the host erythrocyte.
@en
P2093
Janetta G Culvenor
P2860
P304
37658-37663
P356
10.1074/JBC.M305252200
P407
P577
2003-07-11T00:00:00Z