ArticleInterface focus2019
Cell type and receptor identity regulate cholera toxin subunit B (CTB) internalization.
Article in Interface focus, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Immunoinformatic design of a multi-epitope vaccine candidate targeting multidrug-resistant Pseudomonas aeruginosa.BMC immunology · 2026Article
- Retrograde tracing of breast cancer-associated sensory neurons.Journal of microscopy · 2025Article
- Fucosylation of glycoproteins and glycolipids: opposing roles in cholera intoxication.Nature chemical biology · 2025Article
- Vaccine Strategies to Elicit Mucosal Immunity.Vaccines · 2024Review
- Methodological Pitfalls of Investigating Lipid Rafts in the Brain: What Are We Still Missing?Biomolecules · 2024Review
- The diverse landscape of AB5-type toxins.Engineering microbiology · 2023Review
- Cholera intoxication of human enteroids reveals interplay between decoy and functional glycoconjugate ligands.Glycobiology · 2023Article
- Fucosylated glycoproteins and fucosylated glycolipids play opposing roles in cholera intoxication.bioRxiv : the preprint server for biology · 2023Article
- Characterization and utility of two monoclonal antibodies to cholera toxin B subunit.Scientific reports · 2023Article
- The FDA-approved drug Auranofin has a dual inhibitory effect on SARS-CoV-2 entry and NF-κB signaling.iScience · 2022Article
- Mucosal vaccines - fortifying the frontiers.Nature reviews. Immunology · 2022Review
- Cholera Toxin as a Probe for Membrane Biology.Toxins · 2021Review
- Article
- Review
- Fucose-Galactose Polymers Inhibit Cholera Toxin Binding to Fucosylated Structures and Galactose-Dependent Intoxication of Human Enteroids.ACS infectious diseases · 2020Article
- Photocrosslinking probes for capture of carbohydrate interactions.Current opinion in chemical biology · 2019Review
- Crystal structures of cholera toxin in complex with fucosylated receptors point to importance of secondary binding site.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cholera toxin (CT) is a secreted bacterial toxin that binds to glycoconjugate receptors on the surface of mammalian cells, enters mammalian cells through endocytic mechanisms and intoxicates mammalian cells by activating cytosolic adenylate cyclase. CT recognizes cell surface receptors through its B subunit (CTB). While the ganglioside GM1 has been historically described as the sole receptor, CTB is also capable of binding to fucosylated glycoconjugates, and fucosylated molecules have been shown to play a functional role in host cell intoxication by CT. Here, we use colonic epithelial and respiratory epithelial cell lines to examine how two types of CT receptors-gangliosides and fucosylated glycoconjugates-contribute to CTB internalization. We show that fucosylated glycoconjugates contribute to CTB binding to and internalization into host cells, even when the ganglioside GM1 is present. The contributions of the two classes of receptors to CTB internalization depend on cell type. Additionally, in a cell line that harbours both classes of receptors, gangliosides dictate the efficiency of CTB internalization. Together, the results lend support to the idea that fucosylated glycoconjugates play a functional role in CTB internalization, and suggest that CT internalization depends on both receptor identity and cell type.
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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.