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- W2591596104 abstract "ABSTRACT The mRNA-destabilizing factor tristetraprolin (TTP) binds in a sequence-specific manner to the 3′ untranslated regions of many proinflammatory mRNAs and recruits complexes of nucleases to promote rapid mRNA turnover. Mice lacking TTP develop a severe, spontaneous inflammatory syndrome characterized by the overexpression of tumor necrosis factor and other inflammatory mediators. However, TTP also employs the same mechanism to inhibit the expression of the potent anti-inflammatory cytokine interleukin 10 (IL-10). Perturbation of TTP function may therefore have mixed effects on inflammatory responses, either increasing or decreasing the expression of proinflammatory factors via direct or indirect mechanisms. We recently described a knock-in mouse strain in which the substitution of 2 amino acids of the endogenous TTP protein renders it constitutively active as an mRNA-destabilizing factor. Here we investigate the impact on the IL-10-mediated anti-inflammatory response. It is shown that the gain-of-function mutation of TTP impairs IL-10-mediated negative feedback control of macrophage function in vitro . However, the in vivo effects of TTP mutation are uniformly anti-inflammatory despite the decreased expression of IL-10." @default.
- W2591596104 created "2017-03-16" @default.
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- W2591596104 date "2017-06-01" @default.
- W2591596104 modified "2023-10-15" @default.
- W2591596104 title "Gain-of-Function Mutation of Tristetraprolin Impairs Negative Feedback Control of Macrophages <i>In Vitro</i> yet Has Overwhelmingly Anti-Inflammatory Consequences <i>In Vivo</i>" @default.
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- W2591596104 doi "https://doi.org/10.1128/mcb.00536-16" @default.
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