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Journal of Biochemistry Advance Access originally published online on May 26, 2009
Journal of Biochemistry 2009 146(3):375-381; doi:10.1093/jb/mvp080
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© The Authors 2009. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved

TRAF-Interacting Protein with a Forkhead-Associated Domain B (TIFAB) Is a Negative Regulator of the TRAF6-Induced Cellular Functions

Takayuki Matsumura1,2,3, Junko Kawamura-Tsuzuku4, Tadashi Yamamoto4, Kentaro Semba1,2,3 and Jun-ichiro Inoue3,*

1Institute for Biomedical Engineering, Consolidated Research Institute for Advanced Science and Medical Care, Waseda University, Wasedatsurumaki-cho, Shinjuku-ku, Tokyo 162-0041; 2Laboratory of Molecular Oncology, Department of Life Science and Medical Bio-Science, School of Science and Engineering, Waseda University, Wakamatsu-cho, Shinjuku-ku, Tokyo 162-8480; 3Division of Cellular and Molecular Biology; and 4Division of Oncology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan

*To whom correspondence should be addressed. Tel: +81-3-5449-5275, Fax: +81-3-5449-5421, E-mail: jun-i{at}ims.u-tokyo.ac.jp

Received March 6, 2009; Accepted March 18, 2009


  Abstract

Tumour necrosis factor receptor-associated factor (TRAF)-interacting protein with a forkhead-associated domain (TIFA) activates TRAF6 to induce NF-{kappa}B activation. TIFA-related protein, TIFAB, is highly expressed in the spleen and inhibits TIFA-mediated TRAF6 activation. However, little is known about cell types that express TIFAB and its function in those cells. Here, we show that TIFAB is mainly expressed in B cells rather than T cells in the spleen and that the expression level was much higher in dendritic cells (DCs) and macrophages than that in splenic lymphocytes. TIFAB expression was downregulated when B cells, DCs or macrophages were stimulated by TRAF6-mediated proliferative or maturation signals including those emanating from CD40, sIgM and TLRs. Furthermore, microinjection experiments using NIH3T3 cells revealed that TIFAB inhibited entry into the S phase of the cell cycle. Our results suggest that TIFAB could act as a negative regulator of the TRAF6-induced cellular function such as B cell proliferation and maturation of DCs and macrophages.

Key Words: cell cycle, forkhead-associated domain, NF-{kappa}B, TIFA, TRAF

Abbreviations: BrdU, bromodeoxyuridine; FHA, forkhead-associated; HPRT, hypoxanthine phosphoribosyltransferase; NF-{kappa}B, nuclear factor-{kappa}B; TIFA, TRAF-interacting protein with FHA domain; TRAF, tumour necrosis factor receptor-associated factor


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