ArticleInfection and immunity2002
Plasma membrane cholesterol modulates cellular vacuolation induced by the Helicobacter pylori vacuolating cytotoxin.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- SREBF2 enhances lipid metabolism and represses anti-tumor immune responses in cervical cancer by increasing ACAT2.Communications biology · 2026Article
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- Restoration of mitochondrial structure and function withinAdvances in microbiology · 2023Article
- Construction and preservation of a stable and highly expressed recombinant Helicobacter pylori vacuolating cytotoxin A with apoptotic activity.BMC microbiology · 2021Article
- Statins' Regulation of the Virulence Factors ofAntioxidants (Basel, Switzerland) · 2021Review
- Antagonistic Activities ofFrontiers in immunology · 2021Article
- VacA generates a protective intracellular reservoir for Helicobacter pylori that is eliminated by activation of the lysosomal calcium channel TRPML1.Nature microbiology · 2019Article
- Catechin-mediated restructuring of a bacterial toxin inhibits activity.Biochimica et biophysica acta. General subjects · 2019Article
- Dynamic pattern generation in cell membranes: Current insights into membrane organization.Biochimica et biophysica acta. Biomembranes · 2018Review
- Determinants of Raft Partitioning of the Helicobacter pylori Pore-Forming Toxin VacA.Infection and immunity · 2018Article
- Review
- Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense.Current molecular pharmacology · 2017Article
- Cytoplasmic vacuolization in cell death and survival.Oncotarget · 2016Review
- Inhibition of Bacterial Toxin Activity by the Nuclear Stain, DRAQ5™.The Journal of membrane biology · 2016Article
- Review
- Article
- Review
- Inhibition of LtxA toxicity by blocking cholesterol binding with peptides.Molecular oral microbiology · 2016Article
- Cinnamomum verum component 2-methoxycinnamaldehyde: a novel antiproliferative drug inducing cell death through targeting both topoisomerase I and II in human colorectal adenocarcinoma COLO 205 cells.Food & nutrition research · 2016Article
- Discovery of a novel anticancer agent with both anti-topoisomerase I and II activities in hepatocellular carcinoma SK-Hep-1 cells in vitro and in vivo: Cinnamomum verum component 2-methoxycinnamaldehyde.Drug design, development and therapy · 2016Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The Helicobacter pylori vacuolating cytotoxin (VacA) induces the degenerative vacuolation of mammalian cells both in vitro and in vivo. Here, we demonstrate that plasma membrane cholesterol is essential for vacuolation of mammalian cells by VacA. Vacuole biogenesis in multiple cell lines was completely blocked when cholesterol was extracted selectively from the plasma membrane by using beta-cyclodextrins. Moreover, increasing plasma membrane cholesterol levels strongly potentiated VacA-induced vacuolation. In contrast, inhibiting de novo biosynthesis of cholesterol with lovastatin or compactin had no detectable effect on vacuolation. While depletion of plasma membrane cholesterol has been shown to interfere with both clathrin-mediated endocytosis and caveola-dependent endocytosis, neither of these two internalization pathways was found to be essential for vacuolation of cells by VacA. Depleting plasma membrane cholesterol attenuated the entry of VacA into HeLa cells. In addition, beta-cyclodextrin reagents blocked vacuolation of cells that were either preloaded with VacA or had VacA directly expressed within the cytosol. Collectively, our results suggest that plasma membrane cholesterol is important for both the intoxication mechanism of VacA and subsequent vacuole biogenesis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.