Endosomal acidification and activation of NADPH oxidase isoforms are upstream events in hyperosmolarity-induced hepatocyte apoptosis.

@article{Reinehr2006EndosomalAA,
  title={Endosomal acidification and activation of NADPH oxidase isoforms are upstream events in hyperosmolarity-induced hepatocyte apoptosis.},
  author={Roland Reinehr and Stephan Becker and Juliane V Braun and Andrea Eberle and Susanne Grether-Beck and Dieter Ha{\"u}ssinger},
  journal={The Journal of biological chemistry},
  year={2006},
  volume={281 32},
  pages={23150-66}
}
Hyperosmotic exposure of rat hepatocytes induced a rapid oxidative-stress(ROS) response as an upstream signal for proapoptotic CD95 activation. This study shows that hyperosmotic ROS formation involves a rapid ceramide- and protein kinase Czeta (PKCzeta)-dependent serine phosphorylation of p47phox and subsequent activation of NADPH oxidase isoforms. Hyperosmotic p47phox phosphorylation and ROS formation were sensitive to inhibition of sphingomyelinases and were strongly blunted after knockdown… CONTINUE READING

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