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• W1983995711 abstract "The macrophage-mediated inflammatory response is a key etiologic component of obesity-related tissue inflammation and insulin resistance. The transcriptional factor FoxO1 is a key regulator of cell metabolism, cell cycle and cell death. Its activity is tightly regulated by the phosphoinositide-3-kinase-AKT (PI3K-Akt) pathway, which leads to phosphorylation, cytoplasmic retention and inactivation of FoxO1. Here, we show that FoxO1 promotes inflammation by enhancing Tlr4-mediated signalling in mature macrophages. By means of chromatin immunoprecipitation (ChIP) combined with massively parallel sequencing (ChIP-Seq), we show that FoxO1 binds to multiple enhancer-like elements within the Tlr4 gene itself, as well as to sites in a number of Tlr4 signalling pathway genes. While FoxO1 potentiates Tlr4 signalling, activation of the latter induces AKT and subsequently inactivates FoxO1, establishing a self-limiting mechanism of inflammation. Given the central role of macrophage Tlr4 in transducing extrinsic proinflammatory signals, the novel functions for FoxO1 in macrophages as a transcriptional regulator of the Tlr4 gene and its inflammatory pathway, highlights FoxO1 as a key molecular adaptor integrating inflammatory responses in the context of obesity and insulin resistance." @default.
• W1983995711 created "2016-06-24" @default.
• W1983995711 creator A5039839135 @default.
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• W1983995711 date "2010-11-02" @default.
• W1983995711 modified "2023-10-06" @default.
• W1983995711 title "FoxO1 regulates Tlr4 inflammatory pathway signalling in macrophages" @default.
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• W1983995711 doi "https://doi.org/10.1038/emboj.2010.268" @default.
• W1983995711 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3018786" @default.
• W1983995711 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21045807" @default.
• W1983995711 hasPublicationYear "2010" @default.
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