CHOP-mediated hepcidin suppression modulates hepatic iron load - Mueller, Katrin; Sunami, Yoshiaki; Stuetzle, Michael; Guldiken, Nurdan; Kucukoglu, Ozlem; Mueller, Sebastian; Kulaksiz, Hasan; Schwarz, Peggy; Strnad, Pavel (The Journal of pathology, 2013)
Keywords: alcoholic liver disease; Animals; C/EBPα; Carbon Tetrachloride; CCAAT-Enhancer-Binding Protein-alpha - biosynthesis; CCAAT-Enhancer-Binding Protein-alpha - genetics; CHOP; Female; fibrosis; Gene Expression Regulation - drug effects; Gene Knockout Techniques; hepcidin; Hepcidins - biosynthesis; Hepcidins - genetics; Humans; Iron - metabolism; Iron Overload - etiology; Iron Overload - metabolism; Liver - metabolism; Liver Cirrhosis, Experimental - chemically induced; Liver Cirrhosis, Experimental - complications; Liver Cirrhosis, Experimental - metabolism; Liver Diseases, Alcoholic - complications; Liver Diseases, Alcoholic - metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; RNA, Messenger - genetics; Signal Transduction - drug effects; Thioacetamide; Transcription Factor CHOP - biosynthesis; Transcription Factor CHOP - deficiency; Transcription Factor CHOP - genetics; Transcription Factor CHOP - physiology; C/EBPα; CHOP; alcoholic liver disease; hepcidin; fibrosis