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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Hepatocellular-carcinoma; Chemical hepatocarcinogenesis; Protein-kinases; Activation; Mice; Inflammation; Injury; Cell; JNK; Hepatocytes
ISSN (print) / ISBN
1535-6108
e-ISSN
1878-3686
Zeitschrift
Cancer Cell
Quellenangaben
Band: 17,
Heft: 5,
Seiten: 481-496
Verlag
Cell Press
Verlagsort
Cambridge, Mass.
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Virology (VIRO)