| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6093877 | Gastroenterology | 2015 | 17 Pages |
Abstract
We developed mice with liver-specific deletion of ALR, and showed that it is required for mitochondrial function and lipid homeostasis in the liver. ALR-L-KO mice provide a useful model for investigating the pathogenesis of steatohepatitis and its complications.
Keywords
ACACAALRCPTHPCmRNAHCCmessenger RNAROSALDAdenosine TriphosphateATPalcoholic steatohepatitisnonalcoholic steatohepatitisacetyl-CoA carboxylasealcoholic liver diseaseAugmenter of liver regenerationAshNatural killer cellhepatic progenitor cellMouse modelknockoutNash wild typeHepatitis C virusHCVHepatocellular carcinomaReactive oxygen species
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Authors
Chandrashekhar R. Gandhi, J. Richard Chaillet, Michael A. Nalesnik, Sudhir Kumar, Anil Dangi, A. Jake Demetris, Robert Ferrell, Tong Wu, Senad Divanovic, Traci Stankeiwicz, Benjamin Shaffer, Donna B. Stolz, Stephen A.K. Harvey, Jiang Wang,