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Correction for Bibeau-Poirier et al., J Immunol 177 (8) 5059-5067.
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The Journal of Immunology, 2006, 177: 8878-8879.
Copyright © 2006 by The American Association of Immunologists, Inc.

Corrections

Involvement of the I{kappa}B kinase (IKK)-related kinases tank-binding kinase 1/IKKi and cullin-based ubiquitin ligases in IFN regulatory factor-3 degradation

A. Bibeau-Poirier, S.-P. Gravel, J.-F. Clément, S. Rolland, G. Rodier, P. Coulombe, J. Hiscott, N. Grandvaux, S. Meloche and M. J. Servant

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 I{kappa}B 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 IKK{epsilon}. The corrected sentences and Reference 9 are shown below.

These infectious particles activate several kinases in the host including the recently described I{kappa}B kinase (IKK) homologs, IKK{epsilon} (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-IKK{epsilon} 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 beta-actin (clone AC-74) were from Sigma-Aldrich.

9. Peters, R., S. M. Liao, and T. Maniatis. 2000. IKK{epsilon} is part of a novel PMA-inducible I{kappa}B 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.





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