Correction: SUMOylation of Tissue Transglutaminase as Link between Oxidative Stress and Inflammation

Alessandro Luciani; Valeria Rachela Villella; Angela Vasaturo; Ida Giardino; Valeria Raia; Massimo Pettoello-Mantovani; Maria D'Apolito; Stefano Guido; Teresinha Leal; Sonia Quaratino; Luigi Maiuri

doi:10.4049/jimmunol.1490040

Luciani, A., V. R. Villella, A. Vasaturo, I. Giardino, V. Raia, M. Pettoello-Mantovani, M. D'Apolito, S. Guido, T. Leal, S. Quaratino, and L. Maiuri. 2009. SUMOylation of tissue transglutaminase as link between oxidative stress and inflammation. J. Immunol. 183: 2775–2784

The actin bands in Figs. 1E, 2C, and 5E were mistakenly submitted as duplicates of the actin bands in Fig. 3E. This error does not affect the validity of the study or its conclusions. The correct actin bands for Figs. 1E, 2C, and 5E are shown in the revised figures below. The entire figures are reproduced for clarity, but only the actin bands in Figs. 1E, 2C, and 5E have been corrected. The figure legends were correct as published and are shown below for reference.

FIGURE 1.

TG2 SUMOylation in CF airway epithelial cells. A, Immunoblot analysis of SUMO-1 expression in CF IB3-1 and C38 cells. β-actin levels were used as loading control. B, FRET analysis of SUMO-1-TG2 interaction in IB3-1 and C38 cells. C, Immunoprecipitated (IP) TG2 species from whole-cell extracts of IB3-1 cells are immunoreactive for the anti-SUMO-1 Ab. D, Immunoblot analysis of TG2 immunoprecipitates with anti-TG2 Abs. Two TG2 bands are detected in IB3-1 cells. E, Immunoblot analysis of TG2 expression in CF IB3-1 and C38 cells. β-actin levels were used as loading control.

FIGURE 2.

PIASy mediates TG2 SUMOylation in CF airway epithelial cells. A–C, IB3-1 cells were transduced with either human MnSOD or antisense cDNAs in pAd5CMVK vector. A, Immunoblot analysis of TG2 (left) or PIASy (right) immunoprecipitates (IP) with anti-PIASy (left) or anti-TG2 (right) Abs, respectively. B, Immunoblot analysis with anti-SUMO-1 Ab of TG2 immunoprecipitates. C, Immunoblot analysis of SUMO-1, PIASy, and TG2 protein. β-actin levels were used as loading control. D, IB3-1 cells were transfected with either 50 nM human PIASy siRNA or control siRNA. FRET analysis of SUMO-1-TG2 interaction.

FIGURE 5.

Deregulation of ROS machinery mediates TG2 SUMOylation in 16HBE and A549 cells. A and B, 16HBE cell lines were cultured with or without CFTRinh-172 in the presence or absence of MnSOD overexpression. A, FRET analysis reveals SUMO-1-TG2 interaction after CFTR inhibition that was controlled by MnSOD overexpression. B, Immunoblot analysis of PIASy protein. β-actin levels were used as loading control. C and D, A549 cells were cultured with or without rotenone. C, Immunoprecipitated (IP) TG2 species from whole-cell extracts are immunoreactive for the anti-SUMO-1 Ab upon rotenone treatment. D, FRET analysis reveals SUMO-1-TG2 interaction after incubation with rotenone. MnSOD overexpression controls rotenone-induced TG2 SUMOylation. E–G, A549 cells were cultured with H2O2 or under hypoxic conditions. E, Immunoblot analysis of PIASy protein after H2O2 treatment. β-actin levels were used as loading control. F, Immunoblot analysis of TG2 immunoprecipitates (IP) with anti-PIASy Ab after H2O2 treatment in presence or absence of MnSOD overexpression. G, FRET analysis reveals SUMO-1-TG2 interaction after H2O2 treatment as well as when A549 cells were cultured upon hypoxic conditions. The effects of hypoxia on TG2 SUMOylation are controlled by MnSOD overexpression.