ArticleCellular microbiology2011
Shiga toxins induce autophagy leading to differential signalling pathways in toxin-sensitive and toxin-resistant human cells.
Article in Cellular microbiology, 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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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- EnterohemorrhagicAIMS microbiology · 2025Article
- A bacterial toxin co-opts caspase-3 to disable active gasdermin D and limit macrophage pyroptosis.Cell reports · 2024Article
- Epigallocatechin-3-gallate and its nanoformulation in cervical cancer therapy: the role of genes, MicroRNA and DNA methylation patterns.Cancer cell international · 2023Review
- Shiga toxin 2 A-subunit induces mitochondrial damage, mitophagy and apoptosis via the interaction of Tom20 in Caco-2 cells.Heliyon · 2023Article
- Phenotype-Based Threat Assessment.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Green Tea Epigallocatechin-3-Gallate Regulates Autophagy in Male and Female Reproductive Cancer.Frontiers in pharmacology · 2022Review
- Shiga Toxins as Antitumor Tools.Toxins · 2021Review
- Shiga toxin suppresses noncanonical inflammasome responses to cytosolic LPS.Science immunology · 2020Article
- Molecular Biology ofToxins · 2020Review
- Verotoxin-1-Induced ER Stress Triggers Apoptotic or Survival Pathways in Burkitt Lymphoma Cells.Toxins · 2020Article
- Article
- Metabolomic analysis of Shiga toxin 2a-induced injury in conditionally immortalized glomerular endothelial cells.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Suppressing autophagy: a strategy by Escherichia coli O157:H7 for its survival on host epithelial cells.Cell death & disease · 2018Article
- Article
- Review
- Shiga Toxins Activate the NLRP3 Inflammasome Pathway To Promote Both Production of the Proinflammatory Cytokine Interleukin-1β and Apoptotic Cell Death.Infection and immunity · 2016Article
- Phosphorylation of the exchange factor DENND3 by ULK in response to starvation activates Rab12 and induces autophagy.EMBO reports · 2015Article
- Shiga toxins induce autophagic cell death in intestinal epithelial cells via the endoplasmic reticulum stress pathway.Autophagy · 2015Article
- Induction of autophagy in human neuroblastoma SH-SY5Y cells by tri-ortho-cresyl phosphate.Molecular and cellular biochemistry · 2014Article
- DAP1, a negative regulator of autophagy, controls SubAB-mediated apoptosis and autophagy.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The bacterial virulence factors Shiga toxins (Stxs) are expressed by Shigella dysenteriae serotype 1 and certain Escherichia coli strains. Stxs are protein synthesis inhibitors and induce apoptosis in many cell types. Stxs induce apoptosis via prolonged endoplasmic reticulum stress signalling to activate both extrinsic and intrinsic pathways in human myeloid cells. Studies have shown that autophagy, a lysosome-dependent catabolic process, may be associated with activation of pro-survival or death processes. It is currently unknown if autophagy contributes to apoptosis or protects cells from Stxs. To study cellular responses to Stxs, we intoxicated toxin-sensitive cells (THP-1 and HK-2 cells), and toxin-resistant cells (primary human monocyte-derived macrophages) and examined toxin intracellular trafficking and autophagosome formation. Stxs translocated to different cell compartments in toxin-resistant versus toxin-sensitive cells. Confocal microscopy revealed autophagosome formation in both toxin-resistant and toxin-sensitive cells. Proteolytic cleavage of Atg5 and Beclin-1 plays pivotal roles in switching non-cytotoxic autophagy to cell death signalling. We detected cleaved forms of Atg5 and Beclin-1 in Stx-treated toxin-sensitive cells, while cleaved caspases, calpains, Atg5 and Beclin-1 were not detected in toxin-resistant primary human monocytes and macrophages. These findings suggest that toxin sensitivity correlates with caspase and calpain activation, leading to Atg5 and Beclin-1 cleavage.
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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.