Bibeau-Poirier, A., S.-P. Gravel, J.-F. Clément, S. Rolland, G. Rodier, P. Coulombe, J. Hiscott, N. Grandvaux, S. Meloche, and M. J. Servant. 2006. Involvement of the IκB kinase (IKK)-related kinases tank-binding kinase 1/IKKi and cullin-based ubiquitin ligases in IFN regulatory factor-3 degradation. J. Immunol. 177: 5059–5067.
In the first paragraph, fifth sentence of the Introduction and Materials and Methods, and in References, IKKE and IKKe should be IKKε. The corrected sentences and Reference 9 are shown below.
These infectious particles activate several kinases in the host including the recently described IκB kinase (IKK) homologs, IKKε (9), also called IKKi (10), and Tank-binding kinase 1 (TBK1) (11).
Commercial Abs were from the following suppliers: anti-IRF-3 Abs specific for human and rodent species were from Immuno-Biological Laboratories (IBL) and Zymed Laboratories, respectively; anti-IKKε Ab (IMG-270A) (that recognize as well TBK1) was from Imgenex; anti-ubiquitin mAb (clone P4D1) and mAb to MYC were from Santa Cruz Biotechnology; mAbs to hemagglutinin (HA) (clone HA-7) and Flag epitopes and β-actin (clone AC-74) were from Sigma-Aldrich.
9. Peters, R., S. M. Liao, and T. Maniatis. 2000. IKKε is part of a novel PMA-inducible IκB kinase complex. Mol. Cell 5: 513–522.
In Results, in sentence 16 under the heading A Cullin-based ubiquitin ligase pathway is involved in host cell-mediated IRF-3 degradation following SeV infection, reference to CREB coactivator is incorrect. In sentence ten, under the heading Degradation of IRF-3 is dependent of the TBK1/IKKi-signaling pathway; reference to RNA interference silencing technology is incorrect. The corrected sentences are shown below.
Interestingly, this increase in the stability of the hyperphosphorylated forms of IRF-3 was also associated with a sustained activation of IRF-3 as verified by the presence of dimers or its association to CREB binding protein (CBP) coactivator after infection with SeV (Fig. 3E).
We next directly examined the contribution of the IKK-related kinases in IRF-3 degradation by first using RNA interference (RNAi) technology.