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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 
As an example of a comprehensive model of signal transduction, we provide a Wnt network that shows remarkable robustness under a range of phenotypical and pathological conditions. Its simulation allows the clarification of controversially discussed molecular mechanisms of Wnt signalling by predictin...
ORGANISM(S): Homo sapiens (Human) 
2019-11-12 | PXD011835 | Pride
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 
JNK2 inhibits mammary luminal cell commitment
ORGANISM(S): Mus musculus 
2015-10-01 | GSE40226 | GEO
Analysis of JNK-dependent fibroblast-derived soluble factors at gene expression level. The hypothesis tested in the present study was that loss of c-Jun N-terminal kinases 1 and 2, JNK1 and JNK2, in MEFs causes a strong alteration of the gene expression program coding for soluble factors, which prom...
ORGANISM(S): Mus musculus 
JNK2 inhibits mammary luminal cell commitment
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