| First Author | Guo B | Year | 2007 |
| Journal | J Biol Chem | Volume | 282 |
| Issue | 16 | Pages | 11817-26 |
| PubMed ID | 17327220 | Mgi Jnum | J:121134 |
| Mgi Id | MGI:3709423 | Doi | 10.1074/jbc.M700017200 |
| Citation | Guo B, et al. (2007) Modulation of the interferon antiviral response by the TBK1/IKKi adaptor protein TANK. J Biol Chem 282(16):11817-26 |
| abstractText | Induction of type I interferons can be triggered by viral components through Toll-like receptors or intracellular viral receptors such as retinoic acid-inducible gene I. Here, we demonstrate that the TRAF (tumor necrosis factor receptor-associated factor) family member-associated NF-kappaB activator (TANK) plays an important role in interferon induction through both retinoic acid-inducible gene I- and Toll-like receptor-dependent pathways. TANK forms complexes with both upstream signal mediators, such as Cardif/MAVS/IPS-1/VISA, TRIF (Toll-interleukin-1 receptor domain-containing adaptor inducing interferon-beta), and TRAF3 and downstream mediators TANK-binding kinase 1, inducible IkappaB kinase, and interferon regulatory factor 3. In addition, it synergizes with these signaling components in interferon induction. Specific knockdown of TANK results in reduced type I interferon production, increased viral titers, and enhanced cell sensitivity to viral infection. Thus, TANK may be a critical adaptor that regulates the assembly of the TANK-binding kinase 1-inducible IkappaB kinase complex with upstream signaling molecules in multiple antiviral pathways. |
