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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| Main Authors: | , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
05 October 2016
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| 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 |
| 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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