Redox sensitivity of the MyD88 immune signaling adapter

The transcription factor nuclear factor-κB (NF-κB) mediates expression of key genes involved in innate immunity and inflammation. NF-κB activation has been repeatedly reported to be modulated by hydrogen peroxide (H2O2). Here, we show that the NF-κB-activating signaling adapter myeloid differentiati...

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Bibliographic Details
Main Authors: Stottmeier, Benjamin (Author) , Dick, Tobias P. (Author)
Format: Article (Journal)
Language:English
Published: 05 October 2016
In: Free radical biology and medicine
Year: 2016, Volume: 101, Pages: 93-101
ISSN:1873-4596
DOI:10.1016/j.freeradbiomed.2016.10.004
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.freeradbiomed.2016.10.004
Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0891584916304464
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Author Notes:Benjamin Stottmeier, Tobias P. Dick

MARC

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520 |a The transcription factor nuclear factor-κB (NF-κB) mediates expression of key genes involved in innate immunity and inflammation. NF-κB activation has been repeatedly reported to be modulated by hydrogen peroxide (H2O2). Here, we show that the NF-κB-activating signaling adapter myeloid differentiation primary response gene 88 (MyD88) is highly sensitive to oxidation by H2O2 and may be redox-regulated in its function, thus facilitating an influence of H2O2 on the NF-κB signaling pathway. Upon oxidation, MyD88 forms distinct disulfide-linked conjugates which are reduced by the MyD88-interacting oxidoreductase nucleoredoxin (Nrx). MyD88 cysteine residues functionally modulate MyD88-dependent NF-κB activation, suggesting a link between MyD88 thiol oxidation state and immune signaling. 
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