Host but not parasite cholesterol controls Toxoplasma cell entry by modulating organelle discharge.
about
Host cell manipulation by the human pathogen Toxoplasma gondiiRole of cholesterol in parasitic infectionsThe inner membrane complex through development of Toxoplasma gondii and PlasmodiumA Toxoplasma palmitoyl acyl transferase and the palmitoylated armadillo repeat protein TgARO govern apical rhoptry tethering and reveal a critical role for the rhoptries in host cell invasion but not egressEffect of host cell lipid metabolism on alphavirus replication, virion morphogenesis, and infectivityA sporozoite asparagine-rich protein controls initiation of Plasmodium liver stage developmentNa+ Influx Induced by New Antimalarials Causes Rapid Alterations in the Cholesterol Content and Morphology of Plasmodium falciparumPlasmodium falciparum CRK4 directs continuous rounds of DNA replication during schizogonyImmobilization of the type XIV myosin complex in Toxoplasma gondiiA novel co-infection model with Toxoplasma and Chlamydia trachomatis highlights the importance of host cell manipulation for nutrient scavengingThe toxoplasma-host cell junction is anchored to the cell cortex to sustain parasite invasive forceInterrelations between the parasitophorous vacuole of Toxoplasma gondii and host cell organelles.Evidence for host genetic regulation of altered lipid metabolism in experimental toxoplasmosis supported with gene data mining results.Primary intraocular (retinal) lymphoma after ocular toxoplasmosis.Conditional expression of Toxoplasma gondii apical membrane antigen-1 (TgAMA1) demonstrates that TgAMA1 plays a critical role in host cell invasionDeficiency of a Niemann-Pick, type C1-related protein in toxoplasma is associated with multiple lipidoses and increased pathogenicity.Proteomic analysis of rhoptry organelles reveals many novel constituents for host-parasite interactions in Toxoplasma gondii.Interaction of pathogens with host cholesterol metabolismIntroduction of caveolae structural proteins into the protozoan Toxoplasma results in the formation of heterologous caveolae but not caveolar endocytosisVesicles bearing Toxoplasma apicoplast membrane proteins persist following loss of the relict plastid or Golgi body disruption.Neospora caninum Recruits Host Cell Structures to Its Parasitophorous Vacuole and Salvages Lipids from Organelles.Francisella tularensis uses cholesterol and clathrin-based endocytic mechanisms to invade hepatocytes.Eimeria bovis infection modulates endothelial host cell cholesterol metabolism for successful replicationContribution of host lipids to Toxoplasma pathogenesis.Lipidomics of host-pathogen interactions.Recent developments in the interactions between caveolin and pathogens.A Lipolytic Lecithin:Cholesterol Acyltransferase Secreted by Toxoplasma Facilitates Parasite Replication and EgressFierce competition between Toxoplasma and Chlamydia for host cell structures in dually infected cells.Characterization of a second sterol-esterifying enzyme in Toxoplasma highlights the importance of cholesterol storage pathways for the parasiteRhoptries are major players in Toxoplasma gondii invasion and host cell interaction.Toxoplasma gondii salvages sphingolipids from the host Golgi through the rerouting of selected Rab vesicles to the parasitophorous vacuole.Role of an ancestral d-bifunctional protein containing two sterol-carrier protein-2 domains in lipid uptake and trafficking in ToxoplasmaHost cholesterol and inflammation as common key regulators of toxoplasmosis and artherosclerosis development.Host-cell lipid rafts: a safe door for micro-organisms?Targeting of the hydrophobic metabolome by pathogens.CD81 is required for rhoptry discharge during host cell invasion by Plasmodium yoelii sporozoites.Disruption of lipid rafts interferes with the interaction of Toxoplasma gondii with macrophages and epithelial cells.New host nuclear functions are not required for the modifications of the parasitophorous vacuole of Toxoplasma.Toxoplasma depends on lysosomal consumption of autophagosomes for persistent infection.The host cell transcription factor hypoxia-inducible factor 1 is required for Toxoplasma gondii growth and survival at physiological oxygen levels.
P2860
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P2860
Host but not parasite cholesterol controls Toxoplasma cell entry by modulating organelle discharge.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
Host but not parasite choleste ...... odulating organelle discharge.
@ast
Host but not parasite choleste ...... odulating organelle discharge.
@en
type
label
Host but not parasite choleste ...... odulating organelle discharge.
@ast
Host but not parasite choleste ...... odulating organelle discharge.
@en
prefLabel
Host but not parasite choleste ...... odulating organelle discharge.
@ast
Host but not parasite choleste ...... odulating organelle discharge.
@en
P2860
P356
P1476
Host but not parasite choleste ...... modulating organelle discharge
@en
P2093
Isabelle Coppens
P2860
P304
P356
10.1091/MBC.E02-12-0830
P577
2003-05-29T00:00:00Z