Because bile secretion by hepatocytes is apparently mediated by the microfilamentous system of actin, the proposed hormonally induced dysfunction of this system could be translated to cholestasis.
A splice junction mutation causes deletion of a 72-base exon from the mRNA for lysosomal acid lipase in a patient with cholesteryl ester storage disease.
Among the hereditary human cholestasis, a subtype of progressive familial intrahepatic cholestasis with high gamma-glutamyltranspeptidase (GGT) serum activity shares histological, biochemical, and genetic features with mice lacking mdr2 gene expression (mdr2 -/- mice).
Tissue inhibitor of metalloproteinase-1 messenger RNA expression is enhanced relative to interstitial collagenase messenger RNA in experimental liver injury and fibrosis.
We believe that genetic alterations of alpha-1 antitrypsin and P-glycoprotein, either alone or in association with known pathogenetic mechanisms, may explain the onset of danazol induced cholestasis and justify the difference in its varying duration and intensity.
We believe that genetic alterations of alpha-1 antitrypsin and P-glycoprotein, either alone or in association with known pathogenetic mechanisms, may explain the onset of danazol induced cholestasis and justify the difference in its varying duration and intensity.
Its protein product is likely to play an essential role in enterohepatic circulation of bile acids; further characterization of FIC1 will facilitate understanding of normal bile formation and cholestasis.