ArticleBlood2011
Shiga toxin (Stx)1B and Stx2B induce von Willebrand factor secretion from human umbilical vein endothelial cells through different signaling pathways.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 40 citations in OpenAlex.
- Interaction of Shiga toxin with the A-domains and multimers of von Willebrand Factor.The Journal of biological chemistry · 2013Trial
- Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis.Frontiers in immunology · 2026Article
- Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026Article
- The potassium channel KNature communications · 2025Article
- Preventative and therapeutic effects of a novel humanized anti-glycoprotein Ibα fragment of antigen-binding region in a murine model of thrombotic thrombocytopenic purpura.Journal of thrombosis and haemostasis : JTH · 2025Article
- Animal models for thrombotic thrombocytopenic purpura: a narrative review.Annals of blood · 2023Article
- Transformative Materials to Create 3D Functional Human Tissue Models In Vitro in a Reproducible Manner.Advanced healthcare materials · 2023Article
- Application of systems biology to identify pharmacological mechanisms of thrombotic microangiopathy evoked by combined activated prothrombin complex concentrate and emicizumab.Scientific reports · 2023Article
- Exome Sequencing Identifies Abnormalities in Glycosylation and ANKRD36C in Patients with Immune-Mediated Thrombotic Thrombocytopenic Purpura.Thrombosis and haemostasis · 2021Article
- Molecular Biology ofToxins · 2020Review
- Review
- Article
- Bacteriological assessments of foodborne pathogens in poultry meat at different super shops in Dhaka, Bangladesh.Italian journal of food safety · 2019Article
- Sepsis-associated disseminated intravascular coagulation and its differential diagnoses.Journal of intensive care · 2019Review
- Exocytosis of Weibel-Palade bodies: how to unpack a vascular emergency kit.Journal of thrombosis and haemostasis : JTH · 2019Review
- Decreased severity of Shiga toxin-producingBMJ case reports · 2017Article
- Protein kinase A activation by the anti-cancer drugs ABT-737 and thymoquinone is caspase-3-dependent and correlates with platelet inhibition and apoptosis.Cell death & disease · 2017Article
- Article
- Cross-linking of glycosphingolipids at the plasma membrane: consequences for intracellular signaling and traffic.Cellular and molecular life sciences : CMLS · 2016Article
- Syntaxin-binding protein STXBP5 inhibits endothelial exocytosis and promotes platelet secretion.The Journal of clinical investigation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diarrhea-associated hemolytic uremic syndrome (D(+)HUS) is caused by the ingestion of Escherichia coli that produce Shiga toxin (Stx), which is composed of a cytotoxic A subunit and pentameric B subunits that bind globotriaosylceramide on susceptible cells. Stx occurs in 2 types, Stx1 and Stx2. B subunits of either type stimulate von Willebrand factor (VWF) secretion from human umbilical vein endothelial cells (HUVECs), and Stx2B can cause thrombotic microangiopathy in Adamts13(-/-) mice. We have now determined that Stx1B and Stx2B activate different signaling pathways in HUVECs. VWF secretion induced by Stx1B is associated with a transient rise in intracellular Ca(2+) level that is blocked by chelation with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester, removal of extracellular Ca(2+), the phospholipase C inhibitor U73122, the protein kinase inhibitor staurosporine, or small interfering RNA knockdown of protein kinase Cα. In contrast, Stx2B-induced VWF secretion is associated with activation of protein kinase A (PKA) and is blocked by the PKA inhibitor H89 or small interfering RNA knockdown of PKA. Stx2B does not increase cAMP levels and may activate PKA by a cAMP-independent mechanism. The activation of distinct signaling pathways may be relevant to understanding why E coli that express Stx2 are more likely to cause D(+)HUS than are E coli expressing only Stx1.
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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.