First Author | Meena NP | Year | 2016 |
Journal | FEBS Lett | Volume | 590 |
Issue | 10 | Pages | 1498-508 |
PubMed ID | 27086836 | Mgi Jnum | J:233694 |
Mgi Id | MGI:5787866 | Doi | 10.1002/1873-3468.12176 |
Citation | Meena NP, et al. (2016) The TBK1-binding domain of optineurin promotes type I interferon responses. FEBS Lett 590(10):1498-508 |
abstractText | Pathogen-associated molecular pattern (PAMP) recognition leads to TANK-binding kinase (TBK1) polyubiquitination and activation by transautophosphorylation, resulting in IFN-beta production. Here, we describe a mouse model of optineurin insufficiency (OptnDelta(157) ) in which the TBK1-interacting N-terminus of optineurin was deleted. PAMP-stimulated cells from OptnDelta(157) mice had reduced TBK1 activity, no phosphorylation of optineurin Ser(187) , and mounted low IFN-beta responses. In contrast to pull-down assays where the presence of N-terminus was sufficient for TBK1 binding, both the N-terminal and the ubiquitin-binding regions of optineurin were needed for PAMP-induced binding. This report establishes optineurin as a positive regulator TBK1 via a bipartite interaction between these molecules. |