Kelly A. Fader
Affiliations: | 2016- | Michigan State University, East Lansing, MI |
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"Kelly Fader"
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Cholico GN, Orlowska K, Fling RR, et al. (2023) Consequences of reprogramming acetyl-CoA metabolism by 2,3,7,8-tetrachlorodibenzo-p-dioxin in the mouse liver. Scientific Reports. 13: 4138 |
Cholico GN, Fling RR, Zacharewski NA, et al. (2021) Thioesterase induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin results in a futile cycle that inhibits hepatic β-oxidation. Scientific Reports. 11: 15689 |
Fling RR, Doskey CM, Fader KA, et al. (2020) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) dysregulates hepatic one carbon metabolism during the progression of steatosis to steatohepatitis with fibrosis in mice. Scientific Reports. 10: 14831 |
Nault R, Fader KA, Bhattacharya S, et al. (2020) Single nuclei RNA sequencing assessment of the hepatic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Cellular and Molecular Gastroenterology and Hepatology |
Doskey CM, Fader KA, Nault R, et al. (2020) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters hepatic polyunsaturated fatty acid metabolism and eicosanoid biosynthesis in female Sprague-Dawley rats. Toxicology and Applied Pharmacology. 115034 |
Dornbos P, Jurgelewicz A, Fader KA, et al. (2019) Characterizing the Role of HMG-CoA Reductase in Aryl Hydrocarbon Receptor-Mediated Liver Injury in C57BL/6 Mice. Scientific Reports. 9: 15828 |
Fader KA, Nault R, Doskey CM, et al. (2019) 2,3,7,8-Tetrachlorodibenzo-p-dioxin abolishes circadian regulation of hepatic metabolic activity in mice. Scientific Reports. 9: 6514 |
Nault R, Doskey CM, Fader KA, et al. (2018) Comparison of hepatic NRF2 and AHR binding in 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD) treated mice demonstrates NRF2-independent PKM2 induction. Molecular Pharmacology |
Fader KA, Nault R, Raehtz S, et al. (2018) 2,3,7,8-Tetrachlorodibenzo-p-dioxin dose-dependently increases bone mass and decreases marrow adiposity in juvenile mice. Toxicology and Applied Pharmacology |
Fader KA, Nault R, Kirby MP, et al. (2018) Corrigendum to "Convergence of hepcidin deficiency, systemic iron overloading, heme accumulation, and REV-ERBα/β activation in aryl hydrocarbon receptor-elicited hepatotoxicity" [Toxicol Appl Pharmacol. 321 (2017) 1-17]. Toxicology and Applied Pharmacology |