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Am J Physiol Gastrointest Liver Physiol 281: G1279-G1289, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 5, G1279-G1289, November 2001

Dominant-negative TAK1 induces c-Myc and G0 exit in liver

Cynthia A. Bradham, Etsuro Hatano, and David A. Brenner

Departments of Medicine and Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27707

Transforming growth factor-beta (TGF-beta )-activated kinase 1 (TAK1), a serine/threonine kinase, is reported to function in the signaling pathways of TGF-beta , interleukin 1, and ceramide. However, the physiological role of TAK1 in vivo is largely unknown. To assess the function of TAK1 in vivo, dominant-negative TAK1 (dnTAK1) was expressed in the rat liver by adenoviral gene transfer. dnTAK1 expression abrogated c-Jun NH2-terminal kinase and c-Jun but not nuclear factor (NF)-kappa B or SMAD activation after partial hepatectomy (PH). Expression of dnTAK1 or TAM-67, a dominant-negative c-Jun, induced G0 exit in quiescent liver and accelerated cell cycle progression after PH. Finally, dnTAK1 and TAM-67 induced c-myc expression in the liver before and after PH, suggesting that G0 exit induced by dnTAK1 and TAM-67 is mediated by c-myc induction.

partial hepatectomy; proliferation; c-Jun NH2-terminal kinase; transforming growth factor-beta


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