Two recent papers (see below) comment on the importance of Tax binding protein Tax1BP1 and the A20 deubiquitinase for activated NFkB signaling through TRAF6.  An emerging model suggests that K63 ubiquitination of TRAF6 activates NFkB signaling, and that Tax1BP1 recruits A20 to deubiquinate TRAF6 to silence NFkB signaling.  In this context, Tax can be envisioned to prevent Tax1BP1's recruitment of A20; thereby Tax prevents de-Ub of TRAF6 by A20.  Preventing TRAF6 de-ubiquitination is, then, another mechanism through which Tax activates NFkB.

The two relevant papers to consult are:

The EMBO Journal (2007) 26, 3910–3922, doi:10.1038/sj.emboj.7601823 Published online 16 August 2007

Essential role for TAX1BP1 in the termination of TNF--, IL-1- and LPS-mediated NF-B and JNK signaling

Noula Shembade1, Nicole S Harhaj1, Daniel J Liebl2 and Edward W Harhaj1

1 Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, Miller School of Medicine, The University of Miami, Miami, FL, USA 2 The Miami Project to Cure Paralysis and Department of Neurosurgery, Miller School of Medicine, The University of Miami, Miami, FL, USA To whom correspondence should be addressed Edward W Harhaj, Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, Miller School of Medicine, The University of Miami, 1550 NW 10 Avenue, Miami, FL 33136, USA. Tel.: +1 305 243 7893; Fax: +1 305 243 6410; E-mail: eharhaj@med.miami.edu Received 27 February 2007; Accepted 19 July 2007; Published online 16 August 2007.

The EMBO Journal (2008) 27, 629–641, doi:10.1038/emboj.2008.5 Published online 31 January 2008

Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-B activation

Hidekatsu Iha1, 6, 7, Jean-Marie Peloponese1, 7, Lynn Verstrepen2, Grzegorz Zapart3, Fumiyo Ikeda3, C Dahlem Smith4, Matthew F Starost5, Venkat Yedavalli1, Karen Heyninck2, Ivan Dikic3, Rudi Beyaert2 and Kuan-Teh Jeang1

1 Laboratory of Molecular Microbiology, Molecular Virology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA 2 Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, Ghent University—VIB, Ghent (Zwijnaarde), Belgium 3 Institute for Biochemistry II, Goethe University Medical School, Frankfurt, Germany 4 Pathology/Histotechnology Laboratory, SAIC-Frederick Inc., NCI-FCR, Frederick, MD, USA 5 Division of Veterinary Resources, National Institutes of Health, Bethesda, MD, USA 6 Department of Infectious Diseases, Faculty of Medicine, Oita University Idaiga-oka, Hasama Yufu, Japan To whom correspondence should be addressed Kuan-Teh Jeang, Laboratory of Molecular Microbiology, Molecular Virology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 4, Room 306, 9000 Rockville Pike, Bethesda, MD 20892-0460, USA. Tel.: +1 301 496 6680; Fax: +1 301 480 3686; E-mail: kjeang@niaid.nih.gov 7 These authors contributed equally to this work Received 18 September 2007; Accepted 4 January 2008; Published online 31 January 2008.