Hepatocyte-specific c-Met deletion disrupts redox homeostasis and sensitizes to Fas-mediated apoptosis.

@article{GomezQuiroz2008HepatocytespecificCD,
  title={Hepatocyte-specific c-Met deletion disrupts redox homeostasis and sensitizes to Fas-mediated apoptosis.},
  author={Luis Enrique Gomez-Quiroz and Valentina M. Factor and P{\'a}l Kaposi-Nov{\'a}k and C{\'e}dric Coulouarn and Elizabeth A. Conner and Snorri Thorgeirsson},
  journal={The Journal of biological chemistry},
  year={2008},
  volume={283 21},
  pages={14581-9}
}
The hepatocyte growth factor and its receptor c-Met direct a pleiotropic signal transduction pathway that controls cell survival. We previously demonstrated that mice lacking c-Met (Met-KO) in hepatocytes were hypersensitive to Fas-induced liver injury. In this study, we used primary hepatocytes isolated from Met-KO and control (Cre-Ctrl) mice to address more directly the protective effects of c-Met signaling. Loss of c-Met function increased sensitivity to Fas-mediated apoptosis. Hepatocyte… CONTINUE READING
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