Liver-Specific Deletion of SRSF2 Caused Acute Liver Failure and Early Death in Mice.

ABSTRACT: The liver performs a variety of unique functions critical for metabolic homeostasis. Here, we show that mice lacking the splicing factor SRSF2 but not SRSF1 in hepatocytes have severe liver pathology and biochemical abnormalities. Histological analyses revealed generalized hepatitis with the presence of ballooned hepatocytes and evidence of fibrosis. Molecular analysis demonstrated that SRSF2 governs splicing of multiple genes involved in the stress-induced cell death pathway in the liver. More importantly, SRSF2 also functions as a potent transcription activator, required for efficient expression of transcription factors mainly responsible for energy homeostasis and bile acid metabolism in the liver. Consistent with the effects of SRSF2 in gene regulation, accumulation of total cholestero

SUBMITTER: Cheng Y 

PROVIDER: S-EPMC4959313 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature