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Hepatic fibrosis is a wound-healing response to chronic liver injury, which may result in cirrhosis and liver failure. The c-Jun N-terminal kinase-1 (JNK1) gene has been shown to be involved in liver fibrosis. Here, we aimed to investigate the molecular mechanism and identify the cell-type involved ...
ORGANISM(S): Mus musculus 
Chronic liver injury triggers complications such as liver fibrosis and hepatocellular carcinoma (HCC), which are associated with alterations in distinct signaling pathways. Of particular interest is the interaction between mechanisms controlled by IKKγ/NEMO, the regulatory IKK subunit, and Jnk activ...
ORGANISM(S): Mus musculus 
BACKGROUND & AIMS: c-Jun N-terminal kinase (JNK)1 and JNK2 are expressed in hepatocytes and have overlapping and distinct functions. JNK proteins are activated, via phosphorylation, in response to acetaminophen- or CCl4-induced liver damage; the level of activation correlates with the degree of inju...
ORGANISM(S): Mus musculus 
Overexpression of p21 in NEMOM-NM-^Thepa animals protects against DNA damage, acceleration of hepatocarcinogenesis and cholestasis. As strengthened by our LPS stimulation experiments, we identified a novel protective role of p21 against DNA damage. Expression profiling of livers from wild type, NEMO...
ORGANISM(S): Mus musculus 
Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury and cancer. Deletion of NF-ĸB essential modulator in hepatocytes (NemoΔhepa) c...
ORGANISM(S): Mus musculus 
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