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- W3135490595 endingPage "243" @default.
- W3135490595 startingPage "211" @default.
- W3135490595 abstract "Toll-like receptor (TLR) signaling induces substantial changes in the phosphoproteome of innate immune cells, mainly in the form of increased phosphorylation of signaling intermediaries. Loss of constitutive phosphorylation occurs simultaneously, but these transitions from a stable, phosphorylated state in resting cells to a sustained underphosphorylated state in activated cells have received far less attention. This review provides an overview of phosphorylation sites downregulated during TLR-mediated signaling, with a particular focus on TLR4 activation by lipopolysaccharide (LPS). Energy homeostasis, the cell cycle, mitochondrial fission, and gene regulation are among the biological events in macrophages that are regulated through the downregulation of phosphoproteins as part of intracellular signaling events. Phosphoproteomics studies on innate immune cells have identified hundreds of hitherto uncharacterized phosphorylation sites that are lost upon stimulation, indicating that protein hypophosphorylation is a significant, largely unexplored layer of complexity in the TLR4 pathway." @default.
- W3135490595 created "2021-03-15" @default.
- W3135490595 creator A5065957840 @default.
- W3135490595 creator A5074733695 @default.
- W3135490595 date "2021-01-01" @default.
- W3135490595 modified "2023-09-25" @default.
- W3135490595 title "Charting protein dephosphorylation triggered by Toll-like receptor (TLR) signaling in macrophages and its role in health and disease" @default.
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