Functional Genomic Analyses of hepatic tissue after FOXO1 knockout
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE90754 | GEO | 2018/12/01
REPOSITORIES: GEO
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Project description:To explore the molecular mechanism underlying glucose regulation by hepatic FTO, we analyzed transcriptome changes in hepatic tissue after FTO knockout.
2018-12-01 | GSE90687 | GEO
Project description:To explore the molecular mechanism underlying glucose regulation by hepatic FTO, we used the human hepatocyte Hep-G2 cell line as an experimental platform and analyzed transcriptome changes following FTO knock-down.
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Project description:To explore the molecular mechanism underlying glucose regulation by hepatic FTO, we used the human hepatocyte Hep-G2 cell line as an experimental platform and analyzed transcriptome changes following FTO knock-down.
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Project description:Insufficient understanding on cold adaptation technically restricts donor tissue banking. Here we identify FOXO1 as a conserved transcription factor for cell cold survival, relocating from cytosol to nucleus when temperature drops. FOXO1 small ubiquitin-like modifiers (SUMO) -interacting motif (SIM) antagonizes FOXO1-Importin-7 interaction regardless of temperature. At 37°C, SIM enhances FOXO1 interactions with SUMO E3 ligase RANBP2 and Exportin-1, FOXO1 hence cytoplasmic; at 4°C, FOXO1-Importin-7 interaction increases probably via RANBP2, making FOXO1 nuclear. These features enable fine-tuned FOXO1 regulations on chromatin folding and subsequent gene expression. Using these key factors as readouts, a ‘hibernation solution’ was developed, enabling long-term pancreatic islet cold storage and transplantation to cure diabetes. Henceforth, targeting FOXO1 SIM or the SUMO machinery may aid tissue/organ survival from long-term cold and other stresses.
2024-03-01 | GSE183998 | GEO
Project description:Our objective is to determine the role of myeloid FoxO1 in regulating hepatic lipid metabolism and its contribution to nonalcoholic steatohepatitis (NASH) in mice. We generated mice with conditional FoxO1 depletion in myeloid cells, using the FoxO1-LoxP/LysM-Cre system. We then fed myeloid cell-conditional FoxO1-knockout and wild-type male mice a NASH-inducing diet for 25 weeks. Then mice in both groups were euthanized and the liver tissues were procured for the preparation of total RNAs, which were subjected to RNA-seq assay. While myeloid FoxO1 was upregulated in animal models and human subjects with NASH, the underlying mechanism is poorly understood. We found that myeloid cell conditional FoxO1-knockout mice were protected from developing NASH, culminating in the reduction of hepatic inflammation, steatosis and fibrosis. Mechanistically, FoxO1 counteracts Stat6 to skew macrophage polarization from M2 toward M1 signatures to perpetuate hepatic inflammation in NASH. FoxO1 appears as a pivotal mediator of macrophage activation in response to overnutrition and a therapeutic target for ameliorating hepatic inflammation to stem the disease progression from benign steatosis to NASH.
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Project description:Foxo1 is required for proper developmental progression due to distinct functions at different stages of B cell development, but specific gene targets in pro-B cells are not identified. We performed a microarray analysis in v-Abl transformed pro-B cells to compare the gene expression pattern between wildtype and Foxo1 knockout cells. Foxo1f/f-ERCre vAbl transformed pro-B cells were treated with Tamoxifen to delete floxed alleles for 2 days.
2013-04-13 | E-GEOD-46031 | biostudies-arrayexpress
Project description:Foxo1 is required for proper developmental progression due to distinct functions at different stages of B cell development, but specific gene targets in pro-B cells are not identified. We performed a microarray analysis in v-Abl transformed pro-B cells to compare the gene expression pattern between wildtype and Foxo1 knockout cells.
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Project description:RNA-Seq data on livers from 4-5 month old male PiZ mice with or without genetic disruption of insulin receptor and FOXO1 hepatic expression
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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
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