ArticleProceedings of the National Academy of Sciences of the United States of America2003
Anthrax lethal factor represses glucocorticoid and progesterone receptor activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 59 citations in OpenAlex.
- A host defense role for Fibrinogen by direct binding of Clostridium botulinum C2 toxin.Cellular and molecular life sciences : CMLS · 2026Article
- Rapid Discovery and Characterization of Synthetic Neutralizing Antibodies against Anthrax Edema Toxin.Biochemistry · 2019Article
- An overview of anthrax infection including the recently identified form of disease in injection drug users.Intensive care medicine · 2012Review
- Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction.Annals of the New York Academy of Sciences · 2012Review
- Anthrax lethal toxin disrupts the endothelial permeability barrier through blocking p38 signaling.Journal of cellular physiology · 2012Article
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.Infection and immunity · 2011Article
- Respiratory syncytial virus represses glucocorticoid receptor-mediated gene activation.Endocrinology · 2011Article
- Review
- Cellular and systemic effects of anthrax lethal toxin and edema toxin.Molecular aspects of medicine · 2009Review
- Bacillus anthracis lethal toxin represses MMTV promoter activity through transcription factors.Journal of molecular biology · 2009Article
- The role of glucocorticoids and progestins in inflammatory, autoimmune, and infectious disease.Journal of leukocyte biology · 2008Review
- Article
- Differential modulation of glucocorticoid and progesterone receptor transactivation.Molecular and cellular endocrinology · 2008Article
- The large clostridial toxins from Clostridium sordellii and C. difficile repress glucocorticoid receptor activity.Infection and immunity · 2007Article
- Anthrax toxin receptor 2-dependent lethal toxin killing in vivo.PLoS pathogens · 2006Article
- Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens.Nature reviews. Immunology · 2006Review
- Endocrine perturbation increases susceptibility of mice to anthrax lethal toxin.Infection and immunity · 2005Article
- G protein beta interacts with the glucocorticoid receptor and suppresses its transcriptional activity in the nucleus.The Journal of cell biology · 2005Article
- Anthrax lethal toxin induces endothelial barrier dysfunction.The American journal of pathology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We report here that a bacterial toxin, anthrax lethal toxin (LeTx), at very low concentrations represses glucocorticoid receptor (GR) transactivation in a transient transfection system and the activity of an endogenous GR-regulated gene in both a cellular system and an animal model. This repression is noncompetitive and does not affect ligand binding or DNA binding, suggesting that anthrax lethal toxin (LeTx) probably exerts its effects through a cofactor(s) involved in the interaction between GR and the basal transcription machinery. LeTx-nuclear receptor repression is selective, repressing GR, progesterone receptor B (PR-B), and estrogen receptor alpha (ERalpha), but not the mineralocorticoid receptor (MR) or ERbeta. GR repression was also caused by selected p38 mitogen-activated protein (MAP) kinase inhibitors, suggesting that the LeTx action may result in part from its known inactivation of MAP kinases. Simultaneous loss of GR and other nuclear receptor activities could render an animal more susceptible to lethal or toxic effects of anthrax infection by removing the normally protective antiinflammatory effects of these hormones, similar to the increased mortality seen in animals exposed to both GR antagonists and infectious agents or bacterial products. These finding have implications for development of new treatments and prevention of the toxic effects of anthrax.
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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.