Cancer Cell 2017 Sep;32(3):342-359.e10
Department of Pathology and Molecular Pathology, University and University Hospital Zurich, 8091 Zurich, Switzerland. Electronic address:
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Cell Rep 2013 Aug 22;4(4):776-90. Epub 2013 Aug 22.
Department of Medicine III, University Hospital RWTH Aachen, D-52074 Aachen, Germany.
For years, the term "apoptosis" was used synonymously with programmed cell death. However, it was recently discovered that receptor interacting protein 3 (RIP3)-dependent "necroptosis" represents an alternative programmed cell death pathway activated in many inflamed tissues. Here, we show in a genetic model of chronic hepatic inflammation that activation of RIP3 limits immune responses and compensatory proliferation of liver parenchymal cells (LPC) by inhibiting Caspase-8-dependent activation of Jun-(N)-terminal kinase in LPC and nonparenchymal liver cells. Read More
Cell Death Differ 2014 Nov 27;21(11):1721-32. Epub 2014 Jun 27.
Institute for Genetics, Center for Molecular Medicine (CMMC), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Strasse 26, Cologne D-50931, Germany.
Hepatocellular carcinoma (HCC) usually develops in the context of chronic hepatitis triggered by viruses or toxic substances causing hepatocyte death, inflammation and compensatory proliferation of liver cells. Death receptors of the TNFR superfamily regulate cell death and inflammation and are implicated in liver disease and cancer. Liver parenchymal cell-specific ablation of NEMO/IKKγ, a subunit of the IκB kinase (IKK) complex that is essential for the activation of canonical NF-κB signalling, sensitized hepatocytes to apoptosis and caused the spontaneous development of chronic hepatitis and HCC in mice. Read More
Mol Cell Biol 2004 Dec;24(23):10352-65
Department of Basic Medical Sciences, Purdue University, West Lafayette, IN 47907-1246, USA.
Activation of the cellular stress pathways (c-Jun N-terminal kinase [JNK] and p38 mitogen-activated protein [MAP] kinase) is linked to apoptosis. However, whether both pathways are required for apoptosis remains unresolved. Hepatitis B virus X protein (pX) activates p38 MAP kinase and JNK pathways and, in response to weak apoptotic signals, sensitizes hepatocytes to apoptosis. Read More
Cell Death Differ 2016 10 12;23(10):1727-36. Epub 2016 Aug 12.
Centre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
Aberrant cell death/survival has a critical role in the development of hepatocellular carcinoma (HCC). Caspase-2, a cell death protease, limits oxidative stress and chromosomal instability. To study its role in reactive oxygen species (ROS) and DNA damage-induced liver cancer, we assessed diethylnitrosamine (DEN)-mediated tumour development in caspase-2-deficient (Casp2(-/-)) mice. Read More