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- W4362657070A5087156903 rawAffiliation "AAV8-TBG-eGFP, AA8 vector containing enhanced green fluorescent protein coding plasmid under a TBG promoter; AIF, Apoptosis-inducing Factor; ALI, Acute liver injury; ALT, Alanine aminotransferase; APAP, Acetaminophen; Abbreviations: AAV8-TBG-CRE, AA8 vector containing Cre recombinase coding plasmid under a TBG promoter; BAX, Bcl-2-associated X protein; CYP2E1, Cytochrome p45 family 2 subfamily E member 1; DAMPs, Damage associated molecular patterns; DKO, Hepatocyte specific HNF4α-cMyc double knockout; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS; Endo G, Endonuclease G; Funding information: These studies were supported by NIH-COBRE (P20 RR021940-03, P30 GM118247), NIEHS Toxicology Training Grant (T32 ES007079-34), NIH R01 DK0198414 and NIH R56 DK112768; GSH, Glutathione; GSK3β, Glycogen Synthase Kinase 3 Beta; Gclc, Glutamate-Cysteine Ligase Catalytic Subunit; Gclm, Glutamate-Cysteine Ligase Modifier Subunit; H&E, Hematoxylin and eosin; HNF4α, Hepatocyte nuclear factor 4 alpha; HNF4α-KO, Hepatocyte specific HNF4α knockout; IP, Immunoprecipitation; JNK, c-Jun N-terminal kinase; Lay summary: Hepatocyte nuclear factor 4 alpha (HNF4α) is a master regulator of hepatic differentiation and plays important role in proliferation and disease progression. These studies show that maintaining HNF4α expression is essential for liver regeneration to take place after acetaminophen overdose induced acute liver injury. Loss of HNF4α induces cMyc, resulting in inhibition of regeneration and delayed recovery via Nrf2 suppression.; NAPQI, N-acetyl benzoquinone imine; Nqo1, NAD(P)H Quinone Dehydrogenase 1; Nrf2, Nuclear factor-erythroid factor 2-related factor 2; PCNA, Proliferating cell nuclear antigen; PHX, Partial hepatectomy; RIP, Receptor-interacting protein; ROS, Reactive oxygen species; Supplemental Digital Content is available for this article. Direct URL citations are provided in the HTML and PDF versions of this article on the journal's website, www.hepjournal.com.; WT, Wild type; i.p., Intraperitoneal" @default.