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• W2740935106 abstract "Several animal models of Fah deficiency have been developed, including mice, pigs and most recently rats. Initially, the murine models were developed with the intent to mirror the human disease for pathophysiologic and therapeutic studies. However, it soon became apparent that Fah-positive hepatocytes have a potent selective growth advantage in mutant liver and can extensively repopulate the diseased organ. For this reason, Fah mutant mice have become a workhorse for liver biology and are widely used in liver stem cell and hepatic gene therapy research. Immune deficient Fah-knockout mice can be repopulated with human hepatocytes, creating mice with human livers. These chimeric animals have become an important preclinical model for infectious diseases, metabolism and gene therapy. The potent expansion of human hepatocytes in Fah knockout mice has given rise to the concept of using Fah mutants as living bioreactors to produce large quantities of fully mature hepatocytes. As a consequence, larger animal models of Fah deficiency have recently been developed." @default.
• W2740935106 created "2017-08-08" @default.
• W2740935106 creator A5067712261 @default.
• W2740935106 date "2017-01-01" @default.
• W2740935106 modified "2023-10-14" @default.
• W2740935106 title "Fah Knockout Animals as Models for Therapeutic Liver Repopulation" @default.
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• W2740935106 doi "https://doi.org/10.1007/978-3-319-55780-9_20" @default.
• W2740935106 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28755199" @default.
• W2740935106 hasPublicationYear "2017" @default.
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