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J Biol Chem, Vol. 275, Issue 15, 11114-11120, April 14, 2000

Regulatory Mechanisms of TRAF2-mediated Signal Transduction by Bcl10, a MALT Lymphoma-associated Protein^*

Takunari Yoneda^§¶, Kazunori Imaizumi^¶, Mitsuyo Maeda^**, Daishi Yui^¶, Takayuki Manabe^¶, Taiichi Katayama^¶, Naoya Sato^¶, Fumi Gomi^¶, Takashi Morihara^¶§§, Yasutake Mori^¶, Ko Miyoshi^¶§§, Junniti Hitomi^¶, Shinya Ugawa^¶, Shuichi Yamada^¶¶, Masaru Okabe^¶¶, and Masaya Tohyama^¶

From the  Department of Anatomy and Neuroscience,  Department of Ophthalmology, and ^§§ Department of Neuropsychiatry, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871, ^¶ CREST, Japan Science and Technology,  Tanabe Seiyaku Co. Ltd., ^** First Department of Anatomy, Osaka City University Medical School, 1-4-54, Asahimachi, Abeno-ku, Osaka 545-8585, and ^¶¶ Genome Information Research Center, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan

To elucidate the function of Bcl10, recently cloned as an apoptosis-associated gene mutated in MALT lymphoma, we identified its binding partner TRAF2, which mediates signaling via tumor necrosis factor receptors. In mammalian cells, low levels of Bcl10 expression promoted the binding of TRAF2 and c-IAPs. Conversely, excessive expression inhibited complex formation. Overexpressed Bcl10 reduced c-Jun N-terminal kinase activation and induced nuclear factor B activation downstream of TRAF2. To determine whether overexpression of Bcl10 could perturb the regulation of apoptosis in vivo, we generated Bcl10 transgenic mice. In these transgenic mice, atrophy of the thymus and spleen was observed at postnatal stages. The morphological changes in these tissues were caused by acceleration of apoptosis in T cells and B cells. The phenotype of Bcl10 transgenic mice was similar to that of TRAF2-deficient mice reported previously, indicating that excessive expression of Bcl10 might deplete the TRAF2 function. In contrast, in the other organs such as the brain, where Bcl10 was expressed at high levels, no apoptosis was detected. The altered sensitivities to overexpressed Bcl10 may have been due to differences in signal responses to Bcl10 among cell types. Thus, Bcl10 was suggested to play crucial roles in the modulation of apoptosis associated with TRAF2.

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^* This work was supported in part by Ministry of Education, Science, Sports and Culture of Japan.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EMBL Data Bank with accession number(s) AB016069.

^§ To whom correspondence should be addressed. Tel.: 81-6-6879-3221; Fax: 81-6-6879-3229; E-mail: yoneda@anat2.med.osaka-u.ac.jp.

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Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.

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