Bile acid binding proteins in hepatocellular membranes of newborn and adult rats. Identification of transport proteins with azidobenzamidotauro[14C]cholate ([14C]ABATC).

@article{Ziegler1989BileAB,
  title={Bile acid binding proteins in hepatocellular membranes of newborn and adult rats. Identification of transport proteins with azidobenzamidotauro[14C]cholate ([14C]ABATC).},
  author={Kornelia Ziegler and Max Frimmer and Stefan M{\"u}llner and Hugo Fasold},
  journal={Biochimica et biophysica acta},
  year={1989},
  volume={980 2},
  pages={
          161-8
        }
}
17 Citations
The Functional Expression of Sodium-dependent Bile Acid Transport in Madin-Darby Canine Kidney Cells Transfected with the cDNA for Microsomal Epoxide Hydrolase*
TLDR
It is demonstrated that microsomal epoxide hydrolase is expressed on the surface of hepatocytes as well as on transfected MDCK cells and is able to mediate sodium-dependent transport of taurocholate and cholate.
Phylogenic and ontogenic expression of hepatocellular bile acid transport.
TLDR
It is established that the Na+/bile acid cotransport mRNA is first transcribed in mammalian species, a process that is recapitulated late during mammalian fetal development in rat liver, and that this mRNA is lost in dedifferentiated hepatocytes.
Topological photoaffinity labeling of the rabbit ileal Na+/bile-salt-cotransport system.
For the investigation of the topology of the rabbit ileal Na+/bile-salt-cotransport system, composed of a 93-kDa integral membrane protein and a peripheral 14-kDa bile-acid-binding protein (ILBP), we
Identification of Carrier Proteins in Hepatocytes by (Photo) Affinity Labels Derived from Foreign Cyclopeptides
TLDR
The carrier seems to be unable to discriminate between various structurally different compounds like bile acids and cyclopeptides, and was termed a “multispecific transporter” (Ziegler et al. 1985).
Hepatic transport of bile salts.
TLDR
The hepatocyte can regulate expression levels of individual bile salt transporters during cholestasis to evade hepatotoxic injury, and is a vulnerable target for inhibition by estrogen metabolites, drugs such as cyclosporine A, and abnormal bile Salt metabolites, all of which can cause retention of bile salts and consequently intrahepatic cholESTasis.
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TLDR
Analysis of equilibrium data for both cholic and taurocholic acid binding indicates that specific binding is saturable and consistent with Michaelis-Menten kinetics, while nonspecific binding is nonsaturable.
Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats
TLDR
The kinetics of taurocholate uptake by hepatocytes isolated from Sprague-Dawley rats at 7, 14, 21, 28, and 56 days of age suggest that the deficit in hepatic excretory function observed in immature mammals of several species may, in part, be related to decreased transport of bile acids.
Bile-salt-binding polypeptides in plasma membranes of hepatocytes revealed by photoaffinity labelling.
TLDR
Photoaffinity labelling of a membrane subfraction predominantly composed of bile canalicular membranes by the photolabile derivatives of the conjugated bile salts showed covalent incorporation of radioactivity into polypeptides of the same apparent molecular weights as with the subfractions enriched with the sinusoidal membranes.
Hepatocellular uptake of taurocholate in the dog.
  • S. Erlinger
  • Biology, Medicine
    The Journal of clinical investigation
  • 1975
TLDR
The results are consistent with the hypothesis that the uptake of taurocholate is carrier-mediated, and the maximal vilocity of uptake was about six times the known maximal capacity of biliary secretion of taunton in the dog.
Cholic acid uptake and isolated rat hepatocytes.
TLDR
The results suggest that cholic acid is transported by an energy-dependent carrier-mediated process in addition to simple diffusion by hepatocytes, and that the postulated carrier has affinity for other bile acids.
Direct determination of the driving forces for taurocholate uptake into rat liver plasma membrane vesicles.
TLDR
These studies provide definitive evidence for a sodium gradient-dependent, carrier-mediated, electrically neutral transport mechanism for hepatic taurocholate uptake, consistent with a model for bile secretion in which the basolateral enzyme Na+,K+-ATPase provides the driving force for "uphill" bile acid transport by establishing a trans-membrane sodium gradient.
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