Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Eukaryot Cell
2014 Oct 01;1310:1337-45. doi: 10.1128/EC.00088-14.
Show Gene links
Show Anatomy links
Erythrocyte lysis and Xenopus laevis oocyte rupture by recombinant Plasmodium falciparum hemolysin III.
Moonah S
,
Sanders NG
,
Persichetti JK
,
Sullivan DJ
.
???displayArticle.abstract???
Malaria kills more than 1 million people per year worldwide, with severe malaria anemia accounting for the majority of the deaths. Malaria anemia is multifactorial in etiology, including infected erythrocyte destruction and decrease in erythrocyte production, as well as destruction or clearance of noninfected erythrocytes. We identified a panspecies Plasmodium hemolysin type III related to bacterial hemolysins. The identification of a hemolysin III homologue in Plasmodium suggests a potential role in host erythrocyte lysis. Here, we report the first characterization of Plasmodium falciparum hemolysin III, showing that the soluble recombinant P. falciparum hemolysin III is a pore-forming protein capable of lysing human erythrocytes in a dose-, time-, and temperature-dependent fashion. The recombinant P. falciparum hemolysin III-induced hemolysis was partially inhibited by glibenclamide, a known channel antagonist. Studies with polyethylene glycol molecules of different molecular weights indicated a pore size of approximately 3.2 nm. Heterologous expression of recombinant P. falciparum hemolysin III in Xenopus oocytes demonstrated early hypotonic lysis similar to that of the pore-forming aquaporin control. Live fluorescence microscopy localized transfected recombinant green fluorescent protein (GFP)-tagged P. falciparum hemolysin III to the essential digestive vacuole of the P. falciparum parasite. These transfected trophozoites also possessed a swollen digestive vacuole phenotype. Native Plasmodium hemolysin III in the digestive vacuole may contribute to lysis of the parasitophorous vacuole membrane derived from the host erythrocyte. After merozoite egress from infected erythrocytes, remnant P. falciparum hemolysin III released from digestive vacuoles could potentially contribute to lysis of uninfected erythrocytes to contribute to severe life-threatening anemia.
Armstrong,
An FKBP destabilization domain modulates protein levels in Plasmodium falciparum.
2007, Pubmed
Armstrong,
An FKBP destabilization domain modulates protein levels in Plasmodium falciparum.
2007,
Pubmed
Baida,
Cloning and primary structure of a new hemolysin gene from Bacillus cereus.
1995,
Pubmed
Baida,
Mechanism of action of hemolysin III from Bacillus cereus.
1996,
Pubmed
Basler,
Pore-forming and enzymatic activities of Bordetella pertussis adenylate cyclase toxin synergize in promoting lysis of monocytes.
2006,
Pubmed
Casals-Pascual,
Severe malarial anaemia.
2006,
Pubmed
Chen,
Characterization and virulence of hemolysin III from Vibrio vulnificus.
2004,
Pubmed
Chong,
A clinical drug library screen identifies astemizole as an antimalarial agent.
2006,
Pubmed
Coppens,
An update on the rapid advances in malaria parasite cell biology.
2010,
Pubmed
Evans,
Severe malarial anemia of low parasite burden in rodent models results from accelerated clearance of uninfected erythrocytes.
2006,
Pubmed
Gómez,
Deletion of a malaria invasion gene reduces death and anemia, in model hosts.
2011,
Pubmed
Han,
Purification, characterization and molecular cloning of Vibrio fluvialis hemolysin.
2002,
Pubmed
Hewlett,
Macrophage cytotoxicity produced by adenylate cyclase toxin from Bordetella pertussis: more than just making cyclic AMP!
2006,
Pubmed
Jakeman,
Anaemia of acute malaria infections in non-immune patients primarily results from destruction of uninfected erythrocytes.
1999,
Pubmed
Kai,
The pathophysiology of malarial anaemia: where have all the red cells gone?
2008,
Pubmed
Kirk,
Glibenclamide and meglitinide block the transport of low molecular weight solutes into malaria-infected erythrocytes.
1993,
Pubmed
Kissinger,
The Plasmodium genome database.
2002,
Pubmed
Kuronita,
A role for the lysosomal membrane protein LGP85 in the biogenesis and maintenance of endosomal and lysosomal morphology.
2002,
Pubmed
Layez,
Plasmodium falciparum rhoptry protein RSP2 triggers destruction of the erythroid lineage.
2005,
Pubmed
Lee,
Inhibition of Na+-K+ pump and L-type Ca2+ channel by glibenclamide in Guinea pig ventricular myocytes.
2005,
Pubmed
López-Barragán,
Directional gene expression and antisense transcripts in sexual and asexual stages of Plasmodium falciparum.
2011,
Pubmed
Moura,
Role of Plasmodium falciparum digestive vacuole plasmepsins in the specificity and antimalarial mode of action of cysteine and aspartic protease inhibitors.
2009,
Pubmed
Murphy,
Gaps in the childhood malaria burden in Africa: cerebral malaria, neurological sequelae, anemia, respiratory distress, hypoglycemia, and complications of pregnancy.
2001,
Pubmed
Murray,
Global malaria mortality between 1980 and 2010: a systematic analysis.
2012,
Pubmed
Nina,
ATP synthase complex of Plasmodium falciparum: dimeric assembly in mitochondrial membranes and resistance to genetic disruption.
2011,
Pubmed
Nkrumah,
Efficient site-specific integration in Plasmodium falciparum chromosomes mediated by mycobacteriophage Bxb1 integrase.
2006,
Pubmed
Obonyo,
In-hospital morbidity and mortality due to severe malarial anemia in western Kenya.
2007,
Pubmed
Preston,
Appearance of water channels in Xenopus oocytes expressing red cell CHIP28 protein.
1992,
Pubmed
,
Xenbase
Roberts,
The clinical and pathophysiological features of malarial anaemia.
2005,
Pubmed
Robinson,
Adaptable adaptors for coated vesicles.
2004,
Pubmed
Silvestrini,
Protein export marks the early phase of gametocytogenesis of the human malaria parasite Plasmodium falciparum.
2010,
Pubmed
Spalding,
Validation of a modified method for Bxb1 mycobacteriophage integrase-mediated recombination in Plasmodium falciparum by localization of the H-protein of the glycine cleavage complex to the mitochondrion.
2010,
Pubmed
Subramanian,
Falcipain cysteine proteases require bipartite motifs for trafficking to the Plasmodium falciparum food vacuole.
2007,
Pubmed
Tilley,
Illuminating Plasmodium falciparum-infected red blood cells.
2007,
Pubmed
Vignali,
NSR-seq transcriptional profiling enables identification of a gene signature of Plasmodium falciparum parasites infecting children.
2011,
Pubmed
Weatherall,
Malaria and the red cell.
2002,
Pubmed
de Koning-Ward,
A newly discovered protein export machine in malaria parasites.
2009,
Pubmed