Original contributionCharacterization of Hela cell vacuoles induced by Helicobacter pylori broth culture supernatant☆
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Cited by (70)
Mechanisms of Helicobacter pylori-Induced Gastric Inflammation
2018, Physiology of the Gastrointestinal Tract, Sixth EditionHelicobacter pylori vacuolating toxin
2015, The Comprehensive Sourcebook of Bacterial Protein ToxinsHelicobacter pylori VacA: A new perspective on an invasive chloride channel
2012, Microbes and InfectionCitation Excerpt :Autophagy has increasingly been recognized as a means to degrade damaged or dangerous particles in the cells [42–45]. Data concerning an uptake of VacA by autophagic vacuoles were published already in 1992 [46]. However, the relevance of this observation was recognized only recently.
VacA and HP-NAP, Ying and Yang of Helicobacter pylori-associated gastric inflammation
2007, Clinica Chimica ActaHelicobacter pylori vacuolating cytotoxin induces activation of the proapoptotic proteins Bax and Bak, leading to cytochrome c release and cell death, independent of vacuolation
2006, Journal of Biological ChemistryCitation Excerpt :VacA was acid-activated during purification, and its concentrations were calculated based on monomeric forms. Vacuolation was quantified by neutral red accumulation as described by Cover et al. (25). The cells were incubated with freshly prepared 0.05% neutral red in phosphate-buffered saline (PBS) containing 0.3% bovine serum albumin and then washed three times with PBS containing 0.3% bovine serum albumin.
Helicobacter pylori vacuolating toxin
2006, The Comprehensive Sourcebook of Bacterial Protein Toxins
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Supported in part by a grant from The Procter & Gamble Company.
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Dr Cover is a recipient of a Searle Scholars Fellowship Award from the Infectious Disease Society of America.