title: Anthrax mounts a nuclear attack on glucocorticoid signaling.
abstract: Anthrax causes profound inflammation and systemic shock. A recent study has shown that anthrax lethal toxin represses the transcriptional activity of the glucocorticoid receptor, which is a crucial component of the body's defenses against inflammation. The study reports evidence that lethal toxin blocks the glucocorticoid receptor by inhibiting the p38 mitogen-activated protein kinase pathway. Thus, these findings suggest that glucocorticoid receptor inactivation contributes to anthrax toxicity and raise the possibility of developing new strategies to combat this deadly disease.
authors: Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9041, USA. steven.kliewer@utsouthwestern.edu
authors: Steven A
authors: SA
authors: Kliewer
mesh_terms: D000818:Animals; D000881:Anthrax / Q000188:drug therapy / Q000378:metabolism* / Q000382:microbiology; D000942:Antigens, Bacterial / Q000502:physiology; D001408:Bacillus anthracis / Q000502:physiology*; D001427:Bacterial Toxins; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors* / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects*; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D000942:Antigens, Bacterial; D001427:Bacterial Toxins; D011965:Receptors, Glucocorticoid; C030325:anthrax toxin; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases