Hematopoietic cells-derived Jnk1 is crucial for chronic inflammation and carcinogenesis in an experimental model of liver injury

Francisco J. Cubero, Gang Zhao, Yulia A. Nevzorova, Maximilian Hatting, Malika Al Masaoudi, Julien Verdier, Jin Peng, Frederik M. Schaefer, Nadine Hermanns, Mark V. Boekschoten, Christoph Grouls, Nikolaus Gassler, Fabian Kiessling, Michael Muller, Roger J. Davis, Christian Liedtke, Christian Trautwein

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Chronic liver injury triggers complications such as liver fibrosis and hepatocellular carcinoma (HCC), which are associated with alterations in distinct signalling pathways. Of particular interest is the interaction between mechanisms controlled by IKKγ/NEMO, the regulatory IKK subunit, and Jnk activation for directing cell death and survival. In the present study, we aimed to define the relevance of Jnk in hepatocyte-specific NEMO knockout mice (NEMOΔhepa), a genetic model of chronic inflammatory liver injury.
Original languageEnglish
Pages (from-to)140-149
Number of pages10
JournalJournal of Hepatology
Volume62
Issue number1
Early online date1 Aug 2014
DOIs
Publication statusPublished - Jan 2015

Keywords

  • Jnk1
  • Jnk2
  • Necrosis
  • Apoptosis
  • IKKγ/NEMO
  • HCC

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