ATPase Class I Type 8B Member 1 and protein kinase C zeta induce the expression of the canalicular bile salt export pump in human hepatocytes.

ABSTRACT: The exact molecular mechanism(s) of the disease that results from defects in the ATPase Class I Type 8B Member 1 gene remains controversial. Prior investigations of human ileum and in intestinal and ovarian cell lines have suggested that familial intrahepatic cholestasis 1 (FIC1) activates the farnesoid X-receptor (FXR) via a pathway involving protein kinase C zeta (PKCzeta). Translational investigations of human liver from individuals with FIC1 disease have been confounded by secondary affects of progressive cholestatic liver disease and limited numbers of samples for analysis. These studies, performed in primarily derived human hepatocytes, circumvent this issue. The canalicular bile salt export pump (BSEP) served as a downstream target of FXR. The siRNA-mediated silencing of FIC1 in hum

SUBMITTER: Chen F 

PROVIDER: S-EPMC2819672 | biostudies-literature | 2010 Feb

REPOSITORIES: biostudies-literature