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Molecular and Cellular Biology, February 2003, p. 1231-1238, Vol. 23, No. 4
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.4.1231-1238.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

TAB2 Is Essential for Prevention of Apoptosis in Fetal Liver but Not for Interleukin-1 Signaling

Hideki Sanjo,1,2 Kiyoshi Takeda,1,2 Tohru Tsujimura,3 Jun Ninomiya-Tsuji,4 Kunihiro Matsumoto,4 and Shizuo Akira1,2*

Department of Host Defense, Research Institute for Microbial Diseases, Osaka University,1 Solution-Oriented Research for Science and Technology, Japan Science and Technology Corporation, Suita, Osaka 565-0871,2 Department of Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501,3 Department of Molecular Biology, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan4

Received 6 August 2002/ Returned for modification 11 September 2002/ Accepted 15 November 2002

The proinflammatory cytokine interleukin-1 (IL-1) transmits a signal via several critical cytoplasmic proteins such as MyD88, IRAKs and TRAF6. Recently, serine/threonine kinase TAK1 and TAK1 binding protein 1 and 2 (TAB1/2) have been identified as molecules involved in IL-1-induced TRAF6-mediated activation of AP-1 and NF-{kappa}B via mitogen-activated protein (MAP) kinases and I{kappa}B kinases, respectively. However, their physiological functions remain to be clarified. To elucidate their roles in vivo, we generated TAB2-deficient mice. The TAB2 deficiency was embryonic lethal due to liver degeneration and apoptosis. This phenotype was similar to that of NF-{kappa}B p65-, IKKß-, and NEMO/IKK{gamma}-deficient mice. However, the IL-1-induced activation of NF-{kappa}B and MAP kinases was not impaired in TAB2-deficient embryonic fibroblasts. These findings demonstrate that TAB2 is essential for embryonic development through prevention of liver apoptosis but not for the IL-1 receptor-mediated signaling pathway.

* Corresponding author. Mailing address: Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan. Phone: 81-6-6879-8303. Fax: 81-6879-8305. E-mail: sakira{at}biken.osaka-u.ac.jp.

Molecular and Cellular Biology, February 2003, p. 1231-1238, Vol. 23, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.4.1231-1238.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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