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Open Access Green as soon as Postprint is submitted to ZB.
TAK1 suppresses a NEMO-dependent but NF-κB-independent pathway to liver cancer.
Cancer Cell 17, 481-496 (2010)
The MAP3-kinase TGF-beta-activated kinase 1 (TAK1) critically modulates innate and adaptive immune responses and connects cytokine stimulation with activation of inflammatory signaling pathways. Here, we report that conditional ablation of TAK1 in liver parenchymal cells (hepatocytes and cholangiocytes) causes hepatocyte dysplasia and early-onset hepatocarcinogenesis, coinciding with biliary ductopenia and cholestasis. TAK1-mediated cancer suppression is exerted through activating NF-kappaB in response to tumor necrosis factor (TNF) and through preventing Caspase-3-dependent hepatocyte and cholangiocyte apoptosis. Moreover, TAK1 suppresses a procarcinogenic and pronecrotic pathway, which depends on NF-kappaB-independent functions of the I kappaB-kinase (IKK)-subunit NF-kappaB essential modulator (NEMO). Therefore, TAK1 serves as a gatekeeper for a protumorigenic, NF-kappaB-independent function of NEMO in parenchymal liver cells.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Hepatocellular-carcinoma; Chemical hepatocarcinogenesis; Protein-kinases; Activation; Mice; Inflammation; Injury; Cell; JNK; Hepatocytes
ISSN (print) / ISBN
1535-6108
e-ISSN
1878-3686
Journal
Cancer Cell
Quellenangaben
Volume: 17,
Issue: 5,
Pages: 481-496
Publisher
Cell Press
Publishing Place
Cambridge, Mass.
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)