E-GEOD-57804
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA227460PRJNA248130
TISSUE(S): Liver, Aorta
PROVIDER: E-GEOD-57804 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-57804-analysis-methods.tsv | Tabular | |||
| E-GEOD-57804-analytics.tsv | Tabular | |||
| E-GEOD-57804-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-57804-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-57804-analytics.tsv.unrounded | Tabular |
Items per page: 5 1 - 5 of 32 |
Similar Datasets
Project description:Estrogen has vascular protective effects in premenopausal women and in women under 60 receiving hormone replacement therapy. However, estrogen also increases risks of breast and uterine cancers and of venous thromboses linked to upregulation of coagulation factors in the liver. In mouse models, the vasoprotective effects of estrogen are mediated by the estrogen receptor alpha (ERa) transcription factor. Here, through next generation sequencing approaches, we show that almost all of the genes regulated by 17-b-estradiol (E2) differ between mouse aorta and mouse liver, and that this is associated with a distinct genomewide distribution of ERa on chromatin. Bioinformatic analysis of E2-regulated promoters and ERa binding site sequences identify several transcription factors that may determine the tissue specificity of ERa binding and E2-regulated genes, including the enrichment of NFkB, AML1 and AP-1 sites in the promoters of E2 downregulated inflammatory genes in aorta but not liver. The possible vascular-specific functions of these factors suggests ways in which the protective effects of estrogen could be promoted in the vasculature without incurring negative effects in other tissues. Our results also highlight the likely importance of rapid signaling of membrane-associated ERa to cellular kinases (altering the activities of transcription factors other than ER itself) in determining tissue specific transcriptional responses to estrogen.
2014-06-30 | GSE57804 | GEO
Project description:Estrogen has vascular protective effects in premenopausal women and in women under 60 receiving hormone replacement therapy. However, estrogen also increases risks of breast and uterine cancers and of venous thromboses linked to upregulation of coagulation factors in the liver. In mouse models, the vasoprotective effects of estrogen are mediated by the estrogen receptor alpha (ERa) transcription factor. Here, through next generation sequencing approaches, we show that almost all of the genes regulated by 17-b-estradiol (E2) differ between mouse aorta and mouse liver, and that this is associated with a distinct genomewide distribution of ERa on chromatin. Bioinformatic analysis of E2-regulated promoters and ERa binding site sequences identify several transcription factors that may determine the tissue specificity of ERa binding and E2-regulated genes, including the enrichment of NFkB, AML1 and AP-1 sites in the promoters of E2 downregulated inflammatory genes in aorta but not liver. The possible vascular-specific functions of these factors suggests ways in which the protective effects of estrogen could be promoted in the vasculature without incurring negative effects in other tissues. Our results also highlight the likely importance of rapid signaling of membrane-associated ERa to cellular kinases (altering the activities of transcription factors other than ER itself) in determining tissue specific transcriptional responses to estrogen.
2014-06-30 | GSE52351 | GEO
Project description:Estrogen has vascular protective effects in premenopausal women and in women under 60 receiving hormone replacement therapy. However, estrogen also increases risks of breast and uterine cancers and of venous thromboses linked to upregulation of coagulation factors in the liver. In mouse models, the vasoprotective effects of estrogen are mediated by the estrogen receptor alpha (ERa) transcription factor. Here, through next generation sequencing approaches, we show that almost all of the genes regulated by 17-b-estradiol (E2) differ between mouse aorta and mouse liver, and that this is associated with a distinct genomewide distribution of ERa on chromatin. Bioinformatic analysis of E2-regulated promoters and ERa binding site sequences identify several transcription factors that may determine the tissue specificity of ERa binding and E2-regulated genes, including the enrichment of NFkB, AML1 and AP-1 sites in the promoters of E2 downregulated inflammatory genes in aorta but not liver. The possible vascular-specific functions of these factors suggests ways in which the protective effects of estrogen could be promoted in the vasculature without incurring negative effects in other tissues. Our results also highlight the likely importance of rapid signaling of membrane-associated ERa to cellular kinases (altering the activities of transcription factors other than ER itself) in determining tissue specific transcriptional responses to estrogen. The aortas or liver fragments of wild-type C57/BL6 mice were incubated ex vivo with 10nM E2 or ethanol vehicle for 45 minutes before formaldehyde fixation, harvesting of chromatin & ChIP with anti- mouse estrogen receptor alpha antibodies. Each condition was performed with two biological replicates, and each replicate contained aortas or liver fragments from 5 mice.
2014-06-30 | E-GEOD-52351 | biostudies-arrayexpress
Project description:Estrogen has vascular protective effects in premenopausal women and in women under 60 receiving hormone replacement therapy. However, estrogen also increases risks of breast and uterine cancers and of venous thromboses linked to upregulation of coagulation factors in the liver. In mouse models, the vasoprotective effects of estrogen are mediated by the estrogen receptor alpha (ERa) transcription factor. Here, through next generation sequencing approaches, we show that almost all of the genes regulated by 17-b-estradiol (E2) differ between mouse aorta and mouse liver, and that this is associated with a distinct genomewide distribution of ERa on chromatin. Bioinformatic analysis of E2-regulated promoters and ERa binding site sequences identify several transcription factors that may determine the tissue specificity of ERa binding and E2-regulated genes, including the enrichment of NFkB, AML1 and AP-1 sites in the promoters of E2 downregulated inflammatory genes in aorta but not liver. The possible vascular-specific functions of these factors suggests ways in which the protective effects of estrogen could be promoted in the vasculature without incurring negative effects in other tissues. Our results also highlight the likely importance of rapid signaling of membrane-associated ERa to cellular kinases (altering the activities of transcription factors other than ER itself) in determining tissue specific transcriptional responses to estrogen. The aortas or liver fragments of wild-type C57/BL6 mice were incubated ex vivo with 10nM E2 or ethanol vehicle for 4 hours before harvesting for RNA collection. Each condition was performed with two biological replicates, and each replicate contained aortas or liver fragments from 4 mice.
2014-06-30 | E-GEOD-57804 | biostudies-arrayexpress
Project description:To improve our understanding of transcriptional regulation by ESR1 in the liver, chromatin immunoprecipitation with an antibody against ESR1 followed by high-throughput sequencing (ESR1 ChIP-Seq) was conducted in human liver samples and in hepatocytes with or without 17beta-estradiol (E2) treatment. By comparing treated and untreated hepatocytes, we identified both ligand-dependent and ligand-independent binding sites throughout the genome. Ligand-dependent binding sites include ChIP-Seq peaks that either appeared (gained peaks) or disappeared (lost peaks) upon estrogen treatment. Gained peaks occurred at the Estrogen Response Element (ERE) whereas the sites for lost peaks were instead coenriched with a variety of transcription factors. In both cases, ESR1 binding primarily occurred in enhancer regions and was associated with general liver functions, such as lipid/energy metabolism. In contrast, we also observed a subset of ESR1 sites that were maintained regardless of estrogen treatment. These ligand-independent sites mostly occurred at promoter regions and were highly enriched with several cofactor motifs.
2021-02-10 | GSE158856 | GEO
Project description:We performed ChIP seq experiment in MDA-MB-134 cell line in order to map the estrogen receptor alpha (ER) binding sites following the estrogen treatment in an ILC model. We have characterized the genome wide recruit of ER and scaned the binding sites for the presence of cofactor motifs. The binding peaks were also correlated to E2 regulated genes in this ILC model. Four samples were subjected to high throughput sequencing: E-ER (estrogen treated followed by ER IP), E-IgG (estrogen treated followed by IgG), V-ER (EtOH treated followed by ER IP) and Input (MCF7 genomic DNA)
2014-01-15 | E-GEOD-51022 | biostudies-arrayexpress
Project description:We descrive a joint model of transcriptional activation and mRNA accumulation, using estrogen receptor ERM-NM-1 activation in MCF-7 breast cancer cell line, which can be used for inference of transcription rate, RNA processing delay and degradation rate given data from high-throughput sequencing time course experiments. MCF-7 cells were mock treated or with 10nM 17b-E2 to nine time points (5', 10', 20', 40', 80', 160', 320', 640' and 1280'). Genome-wide identification of RNA polymerase II (RNAPII) occupancy and transcriptome profiling (RNA-seq) following E2 induction of MCF-7 cells Please note that the information in the wig.txt files is in gene-specific coordinates, not chromosomic coordinates, as this is the most sensible format for the associated project/paper.
2015-03-04 | E-GEOD-62789 | biostudies-arrayexpress
Project description:High-throughput sequencing of mouse liver transcriptome.
| PRJNA173065 | ENA
Project description:Unopposed estrogen stimulation and insulin resistance are known to play important roles in endometrial cancer (EC), but the relationship between these two factors and how they contribute to endometrial lesions is not completely understood. To investigate the endometrial transcriptome profiles and the associated molecular pathway alterations, we established an ovariectomized C57BL/6 mouse model treated with subcutaneous implantation of the 17-β estradiol (E2) pellet and/or high-fat diet (HFD) to mimic sustained estrogen stimulation and insulin resistance. We used microarrays to detail the global program of gene expression underlying the mice endometrium and indentified distinct classes of E2 and/or high-fat diet related ncRNA during this process.
2018-01-12 | GSE102103 | GEO
Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERα and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERα binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERα, and that ERα binding is increased by E2. Approximately 15% of the uterine ERα binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERα binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERα binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERα to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERα bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERα binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERα and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues.
2012-04-09 | GSE36455 | GEO