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- W2254672185 abstract "Significance Macrophages maintain homeostatic proliferation in the presence of mitogens whereas encounters with invading microorganisms inhibit proliferation and engage a rapid proinflammatory response. Such cell fate change requires an extensive reprogramming of metabolism, and the regulatory mechanisms behind this change remain unknown. We found that myelocytomatosis viral oncogen (Myc) plays a major role in regulating proliferation-associated metabolic programs. However, proinflammatory stimuli suppress Myc and cell proliferation and engage a hypoxia-inducible factor alpha (HIF1α)-dependent transcriptional program that is responsible for heightened glycolysis. Our work indicates that a switch from a Myc-dependent to a HIF1α-dependent transcriptional program may regulate the robust bioenergetic support for inflammatory response, while sparing Myc-dependent proliferation." @default.
- W2254672185 created "2016-06-24" @default.
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- W2254672185 date "2016-01-25" @default.
- W2254672185 modified "2023-10-12" @default.
- W2254672185 title "Proinflammatory signal suppresses proliferation and shifts macrophage metabolism from Myc-dependent to HIF1 <b>α</b> -dependent" @default.
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- W2254672185 doi "https://doi.org/10.1073/pnas.1518000113" @default.
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