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- W2912278776 abstract "Abstract Reactive oxygen species (ROS) production in phagocytes is a major defense mechanism against pathogens. However, the cellular self-protective mechanism against such potential damage from oxidative stress remains unclear. Here we show that the kinases Mst1 and Mst2 (Mst1/2) sense ROS and maintain cellular redox balance by modulating the stability of antioxidant transcription factor Nrf2. Site-specific ROS release recruits Mst1/2 from the cytosol to the phagosomal or mitochondrial membrane, with ROS subsequently activating Mst1/2 to phosphorylate kelch like ECH associated protein 1 (Keap1) and prevent Keap1 polymerization, thereby blocking Nrf2 ubiquitination and degradation to protect cells against oxidative damage. Treatment with the antioxidant N-acetylcysteine disrupts ROS-induced interaction of Mst1/2 with phagosomes or mitochondria, and thereby diminishes the Mst-Nrf2 signal. Consistently, loss of Mst1/2 results in increased oxidative injury, phagocyte ageing and death. Thus, our results identify the Mst-Nrf2 axis as an important ROS-sensing and antioxidant mechanism during an antimicrobial response." @default.
- W2912278776 created "2019-02-21" @default.
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- W2912278776 date "2019-02-14" @default.
- W2912278776 modified "2023-10-10" @default.
- W2912278776 title "Macrophage achieves self-protection against oxidative stress-induced ageing through the Mst-Nrf2 axis" @default.
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- W2912278776 doi "https://doi.org/10.1038/s41467-019-08680-6" @default.
- W2912278776 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6376064" @default.
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- W2912278776 hasPublicationYear "2019" @default.
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