Complement Activation in Acetaminophen-Induced Liver Injury in MiceRohit Singhal, Robert A. Roth|Journal of Pharmacology and Experimental Therapeutics|2012Cited by 52
Trovafloxacin Enhances TNF-Induced Inflammatory Stress and Cell Death Signaling and Reduces TNF Clearance in a Murine Model of Idiosyncratic HepatotoxicityPatrick J. Shaw, Robert A. Roth|Toxicological Sciences|2009Cited by 52
Trovafloxacin Enhances Lipopolysaccharide-Stimulated Production of Tumor Necrosis Factor-α by Macrophages: Role of the DNA Damage ResponseKyle L. Poulsen, Robert A. Roth|Journal of Pharmacology and Experimental Therapeutics|2014Cited by 45
Cytotoxic Synergy Between Cytokines and NSAIDs Associated With Idiosyncratic Hepatotoxicity Is Driven by Mitogen-Activated Protein KinasesAshley R. Maiuri, Robert A. Roth|Toxicological Sciences|2015Cited by 31
Trovafloxacin Potentiation of Lipopolysaccharide-Induced Tumor Necrosis Factor Release from RAW 264.7 Cells Requires Extracellular Signal-Regulated Kinase and c-Jun N-Terminal KinaseKyle L. Poulsen, Robert A. Roth|Journal of Pharmacology and Experimental Therapeutics|2014Cited by 17