Regular ArticleEntamoeba histolytica: Target Cells Killed by Trophozoites Undergo DNA Fragmentation Which Is Not Blocked by Bcl-2
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O-deGlcNAcylation is required for Entamoeba histolytica-induced HepG2 cell death
2018, Microbial PathogenesisCitation Excerpt :Metabolic processes associated with glucose are strongly linked to cell progression and death; however, E. histolytica contact interferes with O-GlcNAcylation processes associated with glucose metabolism. Therefore, E. histolytica-induced host-cell death continues to occur, even following inhibition of caspase or calpain activity or upon Bcl-2 overexpression [8,33]. These findings indicated that E. histolytica accelerates the process of cell death by rapidly and directly disturbing glucose metabolism.
Entamoeba histolytica (Amebiasis)
2018, Principles and Practice of Pediatric Infectious DiseasesInfections of the Liver and Biliary System (Liver Abscess, Cholangitis, Cholecystitis)
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesEntamoeba Species, Including Amebic Colitis and Liver Abscess
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesEfficacy of a Gal-lectin subunit vaccine against experimental Entamoeba histolytica infection and colitis in baboons (Papio sp.)
2012, VaccineCitation Excerpt :Invasive amebiasis was reported in the nineteenth and early twentieth centuries [8–10]; no vaccine is available or has progressed to clinical trial. The pathogenic mechanisms of E. histolytica include contact-dependent cytolysis of mammalian cells [11] and binding by a galactose-inhibitable adherence lectin (Gal-lectin) [11–13]; Gal-lectin binding induces apoptosis o and influx of Ca2+ ions f target cells [14,15]. The Gal-lectin was purified by Petri et al. [13]; the carbohydrate binding site is located on the heavy subunit (1270 amino acids) [16,17].