Withdrawal: Hepatitis C virus NS5A and subgenomic replicon activate NF- κ B via tyrosine phosphorylation of I κ B α and its degradation by calpain protease.

Abstract

Hepatitis C Virus NS5A and Subgenomic Replicon Activate NF-κB via Tyrosine Phosphorylation of IκBα and Its Degradation by Calpain ProteaseJournal of Biological ChemistryVol. 278Issue 42PreviewHepatitis C virus nonstructural protein 5A (NS5A) has been implicated in the HCV antiviral resistance, replication, and transactivation of cellular gene expression. We have recently shown that HCV NS5A activates NF-κB via oxidative stress (22). In this study, we investigate the molecular mechanism(s) of NF-κB activation in response to oxidative stress induced by NS5A protein. In contrast to the classic Ser32,36 phosphorylation of IκBα, we report here that tyrosine phosphorylation of IκBα at Tyr42 and Tyr305 residues is induced by the HCV NS5A and the subgenomic replicons in the NF-κB activation process. Full-Text PDF Open Access VOLUME 278 (2003) PAGES 40778–40787 This article has been withdrawn by the authors. Antonia Livolsi, Véronique Imbert, and Jean-François Peyron participated in the study by providing IκBα mutant plasmids. An investigation by the Journal determined the following. A band was pasted over in the NS5A immunoblot in Fig. 2A. The actin immunoblot from Fig. 2A was reused as actin in 2B, NS5A in 4A, NS5A in 4B, actin in 7D, and actin in 9A. Additionally, this actin immunoblot was reused in the following publications representing different experimental conditions: Waris et al. (2005) J. Virol. 79, 1569–1580, Waris and Siddiqui (2005) J. Virol. 79, 9725–9734, Waris et al. (2007) J. Virol. 81, 8122–8130, Nasimuzzaman et al. (2007) J. Virol. 81, 10249–10257, Burdette et al. (2010) J. Gen. Virol. 91, 681–690, Burdette et al. (2012) J. Gen. Virol. 93, 235–246, Presser et al. (2013) PLOS One 8, e56367, and McRae et al. (2016) J. Biol. Chem. 291, 3254–3267. The EMSA shown in Fig. 3D was reused in Waris et al. (2005) J. Virol. 79, 1569–1580 representing different experimental conditions. Lanes 3 and 5 of the IκBα immunoblot in Fig. 9A were duplicated. The authors who performed the experiments were unable to clarify the Journal’s concerns with original data. Gulam Waris does not agree that the actin immunoblot was reused in other publications. Aleem Siddiqui disagrees with the determination of the reuse of actin immunoblots in publications other than the JBC paper being withdrawn. The authors sincerely apologize to the readers.