Lack of glycoprotein 130/signal transducer and activator of transcription 3-mediated signaling in hepatocytes enhances chronic liver injury and fibrosis progression in a model of sclerosing cholangitis.

@article{Plum2010LackOG,
  title={Lack of glycoprotein 130/signal transducer and activator of transcription 3-mediated signaling in hepatocytes enhances chronic liver injury and fibrosis progression in a model of sclerosing cholangitis.},
  author={Werner Plum and Darjus Felix Tschaharganeh and Daniela C Kroy and Eva Corsten and Stephanie Erschfeld and Uta Dierssen and Hermann Elard Wasmuth and Francisco Javier Cubero and Konrad L. Streetz},
  journal={The American journal of pathology},
  year={2010},
  volume={176 5},
  pages={2236-46}
}
The 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) model leads to chronic cholestatic liver injury and therefore resembles human diseases such as sclerosing cholangitis and forms of metabolic liver diseases. The role of the interleukin-6/glycoprotein 130 (gp130) system in this context is still undefined. Therefore, conditional gp130 knockout and knockin mice were used to achieve hepatocyte-specific deletions of gp130 (gp130(Deltahepa)), gp130-dependent ras (gp130(DeltahepaRas)), and signal… CONTINUE READING
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