ArticleInfection and immunity2011
Glycogen synthase kinase 3 activation is important for anthrax edema toxin-induced dendritic cell maturation and anthrax toxin receptor 2 expression in macrophages.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Effect of a straw-derived xylooligosaccharide on broiler growth performance, endocrine metabolism, and immune response.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2013Trial
- Balancing Immunity: GSK-3's Divergent Roles in Dendritic Cell-Mediated T-Cell Priming and Memory Responses.International journal of molecular sciences · 2025Review
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- Article
- Unique, Intersecting, and Overlapping Roles of C/EBP β and CREB in Cells of the Innate Immune System.Scientific reports · 2018Article
- Endoplasmic reticulum stress induces spatial memory deficits by activating GSK-3.Journal of cellular and molecular medicine · 2018Article
- Cell-penetrating peptides derived fromThe Journal of biological chemistry · 2018Article
- Anthrax Vaccine Precipitated Induces Edema Toxin-Neutralizing, Edema Factor-Specific Antibodies in Human Recipients.Clinical and vaccine immunology : CVI · 2017Article
- 20-HETE attenuates the response of glucose-stimulated insulin secretion through the AKT/GSK-3β/Glut2 pathway.Endocrine · 2016Article
- The Ins and Outs of Anthrax Toxin.Toxins · 2016Review
- Article
- B. anthracis associated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components.BMC medicine · 2013Review
- Increased cAMP in monocytes augments Notch signaling mechanisms by elevating RBP-J and transducin-like enhancer of Split (TLE).The Journal of biological chemistry · 2013Article
- Glycogen synthase kinase 3β inhibition prevents monocyte migration across brain endothelial cells via Rac1-GTPase suppression and down-regulation of active integrin conformation.The American journal of pathology · 2012Article
- Bacillus anthracis edema factor substrate specificity: evidence for new modes of action.Toxins · 2012Review
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- GSK3β and CREB3 gene expression profiling in benign and malignant salivary gland tumors.Iranian biomedical journal · 2012Article
- Regulation by glycogen synthase kinase-3 of inflammation and T cells in CNS diseases.Frontiers in molecular neuroscience · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Anthrax edema toxin (ET) is one of two binary toxins produced by Bacillus anthracis that contributes to the virulence of this pathogen. ET is an adenylate cyclase that generates high levels of cyclic AMP (cAMP), causing alterations in multiple host cell signaling pathways. We previously demonstrated that ET increases cell surface expression of the anthrax toxin receptors (ANTXR) in monocyte-derived cells and promotes dendritic cell (DC) migration toward the lymph node-homing chemokine MIP-3β. In this work, we sought to determine if glycogen synthase kinase 3 (GSK-3) is important for ET-induced modulation of macrophage and DC function. We demonstrate that inhibition of GSK-3 dampens ET-induced maturation and migration processes of monocyte-derived dendritic cells (MDDCs). Additional studies reveal that the ET-induced expression of ANTXR in macrophages was decreased when GSK-3 activity was disrupted with chemical inhibitors or with small interfering RNA (siRNA) targeting GSK-3. Further examination of the ET induction of ANTXR revealed that a dominant negative form of CREB could block the ET induction of ANTXR, suggesting that CREB or a related family member was involved in the upregulation of ANTXR. Because CREB and GSK-3 activity appeared to be important for ET-induced ANTXR expression, the impact of GSK-3 on ET-induced CREB activity was examined in RAW 264.7 cells possessing a CRE-luciferase reporter. As with ANTXR expression, the ET induction of the CRE reporter was decreased by reducing GSK-3 activity. These studies not only provide insight into host pathways targeted by ET but also shed light on interactions between GSK-3 and CREB pathways in host immune cells.
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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.