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MicroRNA-185 modulates CYP7A1 mediated bile acid metabolism through posttranscriptionally and posttranslationally regulation of FoxO1

ABSTRACT: MicroRNA-185 modulates CYP7A1 mediated bile acid metabolism through posttranscriptionally and posttranslationally regulation of FoxO1

PROVIDER: PRJNA717679 | ENA |

REPOSITORIES: ENA

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MicroRNA-185 modulates CYP7A1 mediated bile acid metabolism through posttranscriptionally and posttranslationally regulation of FoxO1

Project description:Cholesterol 7alpha-hydroxylase (CYP7A1) is the rate limiting enzyme of bile acid biosynthetic pathway to convert cholesterol to bile acids, which is a major output pathway for cholesterol catabolism. In this study, we aimed to assess the potential regulatory mechanisms of microRNA-185 (miR-185) involved in cholesterol and bile acid homeostasis. This study provides convincing evidences about the critical role of miR-185 in FoxO1 modulation at both posttranscriptional and posttranslational levels, which account for the effects on CYP7A1 gene and its mediated cholesterol-bile acid metabolism. These results suggest an important role of miR-185 as a novel atherosclerosis-protective target for drug discovery.

2023-03-26 | GSE169693 | GEO

Mortierella sp. AD 185 isolate:AD 185

Project description:Mortierella sp. AD 185 Transcriptome - AD 185

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TDAG51 is a novel coactivator of FoxO1

Project description:Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important in innate immunity. Here, we show that T cell death-associated gene 51 (TDAG51/PHLDA1) is a novel coactivator 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 14-3-3 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 coactivator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response.

2023-06-24 | PXD039815 | Pride

BioID HEK293T PAX3-FOXO1 proximity labelling

Project description:PAX3-FOXO1 is a fusion transcription factor that is the main driver of tumorigenesis leading to the development of alveolar rhabdomyosarcoma (aRMS). Since aRMS cells are addicted to PAX3-FOXO1 activity, the fusion protein also represents a major target for therapeutic interference, which is however challenging as transcription factors usually cannot be inhibited directly by small molecules. Hence, characterization of the biology of PAX3-FOXO1 might lead to the discovery of new possibilities for an indirect inhibition of its activity. Here, our goal was to characterize the proteomic neighborhood of PAX3-FOXO1 and to find candidates potentially affecting its activity and tumor cell viability. Towards this aim, we expressed BirA fused versions of PAX3-FOXO1 (N- and C-terminal) in HEK293T cells under presence of biotin. In the control setup, we expressed the BirA enzyme alone. After Streptavidin purification of biotinylated proteins, we performed mass spectrometry and quantified relative abundances compared to control conditions. This enabled us to determine PAX3-FOXO1 proximal proteins, which we investigated further in orthogonal endogenous systems.

2021-09-16 | PXD022187 | Pride

Streptomyces sp. LaPpAH-185

Project description:Streptomyces sp. LaPpAH-185

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Bile acids and gut motility

Project description:Microbiome-encoded bile acid metabolism modulates colonic transit times

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Streptomyces sp. lappah-185

Project description:Streptomyces sp. LaPpAH-185 genome sequencing

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Acinetobacter lanii strain:185

Project description:Acinetobacter lanii strain:185 Genome sequencing

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Analysis of gene expression changes in endothelial cells upon siRNA of VEGF, Foxo1 or both VEGF+Foxo1

Project description:Analysis of transcriptional changes upon silencing of endothelial VEGF. Because transcription factor Foxo1 levels increase under VEGF silencing, we hypothesized that Foxo1 transcriptional activity would be apparent in a whole-genome microarray. Double-silencing of VEGF+Foxo1 was also performed to determine which transcriptional changes are Foxo1-dependent in a VEGF-deficient background.

2015-12-31 | E-MTAB-2515 | biostudies-arrayexpress

Expression data from Huh7.5 hepatoma cells transfected with 100 nM miR-185 mimic

Project description:Our work demonstrated that 25-hydroxycholesterol induces the expression of miR-185, a microRNA which reinforces the oxysterol's antiviral effects on hepatic metabolism. We used microarrays to detail the effect of miR-185 on hepatic gene expression, and, within repressed genes, identified an enrichment for genes associated with cholesterol biosynthesis.

2015-10-19 | GSE73165 | GEO

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