Anthrax mounts a nuclear attack on glucocorticoid signaling.
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.
Kliewer
Steven A
SA
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9041, USA. steven.kliewer@utsouthwestern.edu
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
D000942:Antigens, Bacterial; D001427:Bacterial Toxins; D011965:Receptors, Glucocorticoid; C030325:anthrax toxin; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases