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Molecular and Cellular Biology, October 1999, p. 6665-6672, Vol. 19, No. 10
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

TANK Potentiates Tumor Necrosis Factor Receptor-Associated Factor-Mediated c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase Activation through the Germinal Center Kinase Pathway

Arnold I-Dah Chin,1 Junyan Shu,2,dagger Chong Shan Shi,3 Zhengbin Yao,4 John H. Kehrl,3 and Genhong Cheng1,2,*

Molecular Biology Institute,1 and Department of Microbiology and Molecular Genetics, Jonsson Comprehensive Cancer Center,2 University of California Los Angeles, Los Angeles, California 90095; B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 208923; and CNS Department, Hoechst Marion Roussel, Bridgewater, New Jersey 088074

Received 31 March 1999/Returned for modification 3 May 1999/Accepted 6 July 1999

Tumor necrosis factor (TNF) receptor-associated factors (TRAFs) are mediators of many members of the TNF receptor superfamily and can activate both the nuclear factor kappa B (NF-kappa B) and stress-activated protein kinase (SAPK; also known as c-Jun N-terminal kinase) signal transduction pathways. We previously described the involvement of a TRAF-interacting molecule, TRAF-associated NF-kappa B activator (TANK), in TRAF2-mediated NF-kappa B activation. Here we show that TANK synergized with TRAF2, TRAF5, and TRAF6 but not with TRAF3 in SAPK activation. TRAF2 and TANK individually formed weak interactions with germinal center kinase (GCK)-related kinase (GCKR). However, when coexpressed, they formed a strong complex with GCKR, thereby providing a potential mechanism for TRAF and TANK synergy in GCKR-mediated SAPK activation, which is important in TNF family receptor signaling. Our results also suggest that TANK can form potential intermolecular as well as intramolecular interactions between its amino terminus and carboxyl terminus. This study suggests that TANK is a regulatory molecule controlling the threshold of NF-kappa B and SAPK activities in response to activation of TNF receptors. In addition, CD40 activated endogenous GCKR in primary B cells, implicating GCK family proteins in CD40-mediated B-cell functions.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095. Phone: (310) 825-8896. Fax: (310) 206-5553. E-mail: genhongc{at}microbio.ucla.edu.

dagger Present address: Department of Medicine, Veteran Affairs West Los Angeles Hospital, Los Angeles, CA 90073.

Molecular and Cellular Biology, October 1999, p. 6665-6672, Vol. 19, No. 10
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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