Effect of FOXO3 on GR Signaling
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786489 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17139500_1.fastq.gz | Fastqsanger.gz | |||
| SRR17139500_2.fastq.gz | Fastqsanger.gz | |||
| SRR17139501_1.fastq.gz | Fastqsanger.gz | |||
| SRR17139501_2.fastq.gz | Fastqsanger.gz | |||
| SRR17139502_1.fastq.gz | Fastqsanger.gz |
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Project description:To identify cross-talk between the transcription factors, glucocorticoid receptor and FOXO3 after activation of the glucocorticoid receptor with dexamethasone.Bone marrow derived macrophages lacking FOXO3 were exposed to vehicle, dexamethasone, a synthetic glucocorticoid.
2022-11-18 | GSE190235 | GEO
Project description:Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter results in disulfide formation between protein (hetero)dimers that alter protein function until the cellular redox has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the FOXO4 transcription factor. Here, we present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptor IPO7 forms a disulfide-dependent heterodimer with FOXO3, but not with FOXO4, which is required for reactive oxygen species (ROS)-induced nuclear translocation . These findings suggest that evolutionary acquisition of cysteines has contributed to functional divergence of FOXO paralogs.
2014-08-26 | PXD001040 | Pride
Project description:Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter results in disulfide formation between protein (hetero)dimers that alter protein function until the cellular redox has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the FOXO4 transcription factor. Here, we present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptor IPO7 forms a disulfide-dependent heterodimer with FOXO3, but not with FOXO4, which is required for reactive oxygen species (ROS)-induced nuclear translocation . These findings suggest that evolutionary acquisition of cysteines has contributed to functional divergence of FOXO paralogs.
2014-08-26 | PXD001018 | Pride
Project description:Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter results in disulfide formation between protein (hetero)dimers that alter protein function until the cellular redox has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the FOXO4 transcription factor. Here, we present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptor IPO7 forms a disulfide-dependent heterodimer with FOXO3, but not with FOXO4, which is required for reactive oxygen species (ROS)-induced nuclear translocation . These findings suggest that evolutionary acquisition of cysteines has contributed to functional divergence of FOXO paralogs.
2014-08-26 | PXD001041 | Pride
Project description:Activation of hepatic FoxO3 signaling induces hyperglycemia and hyperinsulinemia. Metformin administration reverses FoxO3-induced phenotype development. To investigate the underlying mechanism, we used microarrays to detail the global programme of gene expression which is regulated by hepatic FoxO3 signaling.
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Project description:FOXO transcription factors are key players in diverse cellular responses affecting tumorigenesis, stem cell maintenance and lifespan. To gain insight into mechanisms of FOXO regulated gene expression, we studied genome-wide effects of FOXO3 activation. Profiling RNA polymerase II (RNAPII) changes shows FOXO3 regulates gene expression through transcription initiation. Correlative analysis of FOXO3 and RNAPII ChIP-seq profiles demonstrates FOXO3 to act as a transcriptional activator. Furthermore, this analysis reveals a significant part of FOXO3 gene regulation proceeds through enhancer regions. FOXO3 binds to and activates enhancers as shown by the presence of and changes in enhancer-specific histone modifications and RNAPII occupancy. In addition, FOXO3-mediated enhancer regulation correlates with regulation of adjacent genes and existence of chromatin loops between FOXO3 bound enhancers and regulated genes. Combined, our data elucidate how FOXOs regulate gene transcription and provide insight into mechanisms by which FOXOs can induce different gene expression programs depending on chromatin architecture. seven 4C view point were analyzed on DLD1 colon carcinoma cells containing 4OH-Tamoxifen inducible FOXO3A3-ER (DL23 cells, Kops et al., 2002, Mol Cell Biol), to investigate 3D topology around FOXO3 bound regions and FOXO3 regulated genes before and 4 hours after addition of tamoxifen. 4C procedure, as published before (Splinter et al., 2001, Genes Dev). Cells are cross linked using 1% formaldehyde for 10min at room temperature, nuclei are isolated, after which chromatin is digested with DpnII and subsequently ligated under diluted conditions. After reversal of the cross links the DNA is purified and treated with the second restriction enzyme treatment (Csp). After a second re-ligation step the sample is purified and ligated fragments are analyzed by inverse PCR.
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Project description:The effect of exposure to neighborhood violence on GR signaling in lung tumors [Spatial Transcriptomics]
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Project description:The effect of exposure to neighborhood violence on GR signaling in lung tumors [CUT&Run]
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Project description:Despite lower rates and intensity of smoking, Black men experience a higher incidence of lung cancer compared to White men. The racial disparity in lung cancer is particularly pronounced in Chicago, a highly segregated urban city. Neighborhood conditions, particularly social stress, may play a role in lung tumorigenesis. Preliminary studies indicate that Black men residing in neighborhoods with higher rates of violent crime have significantly higher levels of hair cortisol, an indicator of stress response. To examine the relationship between social stress exposure and gene expression in lung tumors, we investigated glucocorticoid receptor (GR) binding in lung tumor samples in relation to GR target gene expression levels and zip code level residential neighborhood violence. Spatial transcriptomics and a version of ChIP-sequencing known as CUT & RUN were used. GR recruitment to chromatin was correlated with neighborhood violent crime rate and overall GR binding increased with increasing neighborhood violent crime rates. Among patients residing in high-violence neighborhoods, tumor samples, compared to normal neighboring lung tissue, had fewer GR binding sites. The opposite was seen in patients residing in low-violence neighborhoods, with tumor samples having more GR binding sites when compared to normal lung tissue. Tumor samples from patients living in high-violence neighborhoods exhibited increased GR recruitment to genes associated with greater tumor aggressiveness. Our findings suggest that exposure to neighborhood violence may influence tumor biology via reprogramming GR recruitment. Prioritizing lung cancer screening in neighborhoods with increased social stress, such as high violence, may reduce racial disparities in lung cancer.
2024-07-10 | GSE268048 | GEO
Project description:FOXO transcription factors are key players in diverse cellular responses affecting tumorigenesis, stem cell maintenance and lifespan. To gain insight into mechanisms of FOXO regulated gene expression, we studied genome-wide effects of FOXO3 activation. Profiling RNA polymerase II (RNAPII) changes shows FOXO3 regulates gene expression through transcription initiation. Correlative analysis of FOXO3 and RNAPII ChIP-seq profiles demonstrates FOXO3 to act as a transcriptional activator. Furthermore, this analysis reveals a significant part of FOXO3 gene regulation proceeds through enhancer regions. FOXO3 binds to and activates enhancers as shown by the presence of and changes in enhancer-specific histone modifications and RNAPII occupancy. In addition, FOXO3-mediated enhancer regulation correlates with regulation of adjacent genes and existence of chromatin loops between FOXO3 bound enhancers and regulated genes. Combined, our data elucidate how FOXOs regulate gene transcription and provide insight into mechanisms by which FOXOs can induce different gene expression programs depending on chromatin architecture.
2012-12-30 | GSE36835 | GEO