MicroRNA-561 Promotes Acetaminophen-Induced Hepatotoxicity in Hepg2 Cells and Primary Human Hepatocytes through Down-Regulation of the Nuclear Receptor Co-Repressor Dosage-Sensitive Sex Reversal Adrenal Hypoplasia Congenital Critical Region on X Chromosome, Gene 1 (DAX-1)
نویسندگان
چکیده
Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL 33612 (M Li, ZW Zhou, & SF Zhou) Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, Yinchuan City, Ningxia Hui Autonomous Region 750004, China (Y Yang) Guizhou Provincial Key Lab for Regenerative Medicine, Stem Cell and Tissue Engineering Research Center, Guiyang Medical University, Guiyang 550004, Guizhou, China (ZX He) Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, UT 84132 (T Yang) Nanobiotechnology Center & Markey Cancer Center, College of Pharmacy, University of Kentucky, Lexington, KY 40536 (P Guo). Research Center for Bioengineering and Sensing Technology, University of Science and Technology Beijing, Beijing 100083, China (X Zhang). DMD Fast Forward. Published on October 8, 2013 as doi:10.1124/dmd.113.052670
منابع مشابه
Dmd052670 44..61
One of the major mechanisms involved in acetaminophen (APAP)induced hepatotoxicity is hepatocyte nuclear factor 4a (HNF4a)mediated activation of pregnane X receptor (PXR) and constitutive androstane receptor (CAR). In the present study, we investigated the role of miR-561 and its target gene DAX-1 encoding a corepressor of HNF4a in the process of APAP-induced hepatotoxicity. We used both human ...
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