MassIVE MSV000092336

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Protein Modifications Driven by Nitric Oxide and Nitroxyl during Macrophage Proinflammatory Activation

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Description

Proinlfammatory stimulation of murine macrophages elicits profound metabolic changes. iNOS-derived Nitric oxide (NO) is both necessary and sufficient for the repression of OXPHOS and major mitochondrial rewiring of carbon fluxes during M1 polarization. Since inflammation results in broad proteomics changes with oxidative modifications of specific targets, we aim to understand how this is managed in absence of this important endogenous gas and its derived reductive nitrogen species like nitroxyl (HNO). We used proteomics to detail the mitochondrial proteome expression and status of cysteine modifications underlying proinflammatory stimulation and identified distinct targets of reversible and irreversible cysteine oxidations during this process in presence and absence of NOS2, RNS donors, and in exacerbating conditions of oxidative stress. [doi:10.25345/C5JM23S00] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: macrophage, nitric oxide, nitroxyl, irreversible modification, free cysteines, inflammation, nitrosative stress

Contact

Principal Investigators:
(in alphabetical order) 		Daniel McVicar, National Cancer Institute (NCI), United States
Submitting User: ronholes7059
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