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Corrigendum: the role played by mitochondria in fcϵri-dependent mast cell activation

A Corrigendum on

By Chelombitko MA, Chernyak BV, Fedorov AV, Zinovkin RA, Razin E and Paruchuru LB (2020). Front. Immunol. 11: 584210. doi:

In the original article, there was an error. The statement that mitochondrial ROS inhibit the activity of NEMO is wrong. Mitochondrial ROS are crucial for the activation of the IKK-NEMO complex.

A correction has been made to the sectionThe Role Played by Mitochondria in the FcϵRI-Dependent Mast Cell Activation, subsectionMitochondrial ROS, paragraph 6. The correct paragraph appears below.

Mitochondrial ROS can stimulate NF-κB signaling by activating the kinase (IKK) of the inhibitor of NF-κB (IκB), which promotes its proteasome degradation and induces nuclear translocation of NF-κB ( 81 , 84 ). Mitochondrial ROS-dependent activation of IKK can be mediated by several mechanisms, including the formation of intermolecular disulfide bonds in NF-κB essential modulator (NEMO), a component of the IKK complex ( 85 ).

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

References

81. Park J, Min J-S, Kim B, Chae U-B, Yun JW, Choi M-S, et al. Mitochondrial ROS govern the LPS-induced pro-inflammatory response in microglia cells by regulating MAPK and NF-κB pathways. Neurosci Lett.(2015) 584: 191–196. doi: 10. 1016/j. neulet. 2014. 10. 016

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84. Zinovkin RA, Romaschenko VP, Galkin II, Zakharova VV, Pletjushkina OY, Chernyak BV, et al. Role of mitochondrial reactive oxygen species in age-related inflammatory activation of endothelium. Aging . (2014) 6: 661–74. doi: 10. 18632/aging. 100685

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85. Herb M, Gluschko A, Wiegmann K, Farid A, Wolf A, Utermöhlen O, et al. Mitochondrial reactive oxygen species enable proinflammatory signaling through disulfide linkage of NEMO. Sci Signal . (2019) 12: eaar5926. doi: 10. 1126/scisignal. aar5926

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