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- W4377094782 abstract "Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important for innate immunity. Here, we show that T-cell death-associated gene 51 (TDAG51/PHLDA1) is a novel regulator of the transcription factor FoxO1, regulating inflammatory mediator production in the lipopolysaccharide (LPS)-induced inflammatory response. TDAG51 induction by LPS stimulation was mediated by the TLR2/4 signaling pathway in bone marrow-derived macrophages (BMMs). LPS-induced inflammatory mediator production was significantly decreased in TDAG51-deficient BMMs. In TDAG51-deficient mice, LPS- or pathogenic Escherichia coli infection-induced lethal shock was reduced by decreasing serum proinflammatory cytokine levels. The recruitment of 14-3-3ζ to FoxO1 was competitively inhibited by the TDAG51-FoxO1 interaction, leading to blockade of FoxO1 cytoplasmic translocation and thereby strengthening FoxO1 nuclear accumulation. TDAG51/FoxO1 double-deficient BMMs showed significantly reduced inflammatory mediator production compared with TDAG51- or FoxO1-deficient BMMs. TDAG51/FoxO1 double deficiency protected mice against LPS- or pathogenic E. coli infection-induced lethal shock by weakening the systemic inflammatory response. Thus, these results indicate that TDAG51 acts as a regulator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response." @default.
- W4377094782 created "2023-05-20" @default.
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- W4377094782 date "2023-05-19" @default.
- W4377094782 modified "2023-10-02" @default.
- W4377094782 title "<scp>TDAG51</scp> promotes transcription factor <scp>FoxO1</scp> activity during <scp>LPS</scp>‐induced inflammatory responses" @default.
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- W4377094782 doi "https://doi.org/10.15252/embj.2022111867" @default.
- W4377094782 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37203866" @default.
- W4377094782 hasPublicationYear "2023" @default.
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