Bcl2 is a critical regulator of bile acid homeostasis by dictating Shp and lncRNA H19 function

• Published in: Scientific reports Vol. 6; no. 1; p. 20559
• Main Authors: Zhang, Yuxia, Liu, Chune, Barbier, Olivier, Smalling, Rana, Tsuchiya, Hiroyuki, Lee, Sangmin, Delker, Don, Zou, An, Hagedorn, Curt H., Wang, Li
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 03.02.2016; Nature Publishing Group
• Subjects: 13/106; 13/95; 45; 45/91; 59; 631/80/304; 692/4020/4021/288/2032; Animals; Bile; Bile Acids and Salts - blood; Bile Acids and Salts - metabolism; Bilirubin; Biodegradation; Caspase; Caspase 8 - metabolism; Caspase-8; Cell Line; Disease Models, Animal; Enzymes; Fibrosis; Gene Expression Regulation; Gene silencing; Gene transfer; HeLa Cells; Hep G2 Cells; Homeostasis; HT29 Cells; Humanities and Social Sciences; Humans; Liver; Liver - metabolism; Liver Diseases - metabolism; Liver Diseases - pathology; Mice; multidisciplinary; Non-coding RNA; Proto-Oncogene Proteins c-bcl-2 - metabolism; Receptors, Cytoplasmic and Nuclear - metabolism; RNA, Long Noncoding - metabolism; Rodents; Science; Signal Transduction

Bile acid (BA) metabolism is tightly controlled by nuclear receptor signaling to coordinate regulation of BA synthetic enzymes and transporters. Here we reveal a molecular cascade consisting of the antiapoptotic protein BCL2, nuclear receptor Shp and long non-coding RNA (lncRNA) H19 to maintain BA h...