Anthrax lethal toxin enhances TNF-induced endothelial VCAM-1 expression via an IFN regulatory factor-1-dependent mechanism.

PubWeight™: 0.92‹?›

🔗 View Article (PMID 18490752)

Published in J Immunol on June 01, 2008

Authors

Jason M Warfel1, Felice D'Agnillo

Author Affiliations

1: Laboratory of Biochemistry and Vascular Biology, Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892.

Articles citing this

Cellular and systemic effects of anthrax lethal toxin and edema toxin. Mol Aspects Med (2009) 2.93

Gram-positive and gram-negative bacterial toxins in sepsis: a brief review. Virulence (2013) 1.08

IRF-1 and miRNA126 modulate VCAM-1 expression in response to a high-fat meal. Circ Res (2012) 1.04

Gene expression profiling of human alveolar macrophages infected by B. anthracis spores demonstrates TNF-alpha and NF-kappab are key components of the innate immune response to the pathogen. BMC Infect Dis (2009) 0.93

The effects of anthrax lethal toxin on host barrier function. Toxins (Basel) (2011) 0.86

Anthrax lethal toxin downregulates claudin-5 expression in human endothelial tight junctions. PLoS One (2013) 0.84

Anthrax lethal toxin-mediated disruption of endothelial VE-cadherin is attenuated by inhibition of the Rho-associated kinase pathway. Toxins (Basel) (2011) 0.82

Scorpion venom component III inhibits cell proliferation by modulating NF-κB activation in human leukemia cells. Exp Ther Med (2012) 0.78

The Rho-GEF Trio regulates a novel pro-inflammatory pathway through the transcription factor Ets2. Biol Open (2013) 0.78

Anthrax lethal toxin enhances IkappaB kinase activation and differentially regulates pro-inflammatory genes in human endothelium. J Biol Chem (2009) 0.78

Bacillus anthracis lethal toxin represses MMTV promoter activity through transcription factors. J Mol Biol (2009) 0.76

Development of an in vitro potency assay for anti-anthrax lethal toxin neutralizing antibodies. Toxins (Basel) (2012) 0.75

Articles by these authors

Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy. J Clin Invest (2012) 2.19

Cellular prion protein is expressed on endothelial cells and is released during apoptosis on membrane microparticles found in human plasma. Transfusion (2002) 2.18

Anthrax lethal toxin induces endothelial barrier dysfunction. Am J Pathol (2005) 1.81

Sequestration of extracellular hemoglobin within a haptoglobin complex decreases its hypertensive and oxidative effects in dogs and guinea pigs. J Clin Invest (2009) 1.77

First-generation blood substitutes: what have we learned? Biochemical and physiological perspectives. Expert Opin Biol Ther (2007) 1.13

Effects of endogenous ascorbate on oxidation, oxygenation, and toxicokinetics of cell-free modified hemoglobin after exchange transfusion in rat and guinea pig. J Pharmacol Exp Ther (2007) 1.11

Hemoglobin-based oxygen carriers: From mechanisms of toxicity and clearance to rational drug design. Trends Mol Med (2010) 1.09

Toxicological consequences of extracellular hemoglobin: biochemical and physiological perspectives. Antioxid Redox Signal (2010) 1.07

Differential induction of renal heme oxygenase and ferritin in ascorbate and nonascorbate producing species transfused with modified cell-free hemoglobin. Antioxid Redox Signal (2010) 0.95

Blood-brain barrier disruption and oxidative stress in guinea pig after systemic exposure to modified cell-free hemoglobin. Am J Pathol (2011) 0.92

Anthrax lethal toxin enhances cytokine-induced VCAM-1 expression on human endothelial cells. Biochem Biophys Res Commun (2005) 0.83

Anthrax lethal toxin-mediated disruption of endothelial VE-cadherin is attenuated by inhibition of the Rho-associated kinase pathway. Toxins (Basel) (2011) 0.82

Sodium nitrite induces acute central nervous system toxicity in guinea pigs exposed to systemic cell-free hemoglobin. Biochem Biophys Res Commun (2011) 0.79

Anthrax lethal toxin enhances IkappaB kinase activation and differentially regulates pro-inflammatory genes in human endothelium. J Biol Chem (2009) 0.78

The large clostridial toxins from Clostridium sordellii and C. difficile repress glucocorticoid receptor activity. Infect Immun (2007) 0.78