Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23370943_1.fastq.gz | Fastqsanger.gz | |||
| SRR23370943_2.fastq.gz | Fastqsanger.gz | |||
| SRR23370944_1.fastq.gz | Fastqsanger.gz | |||
| SRR23370944_2.fastq.gz | Fastqsanger.gz | |||
| SRR23370945_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:The goal of this study was to identify genomic binding sites of the SF-1 nuclear receptor under conditions of basal and increased dosage in the H295R human adrenocortical tumor cell line. 14 samples: input DNA (2 replicates) - SF-1 ChIP Millipore antibody basal SF-1 dosage (3 replicates) - SF-1 ChIP Millipore antibody increased SF-1 dosage (3 replicates) - SF-1 ChIP Perseus antibody basal SF-1 dosage (3 replicates) - SF-1 ChIP Perseus antibody increased SF-1 dosage (3 replicates)
2013-08-01 | E-GEOD-44220 | biostudies-arrayexpress
Project description:The goal of this study was to identify chromatin regulatory sites by FAIRE-seq under conditions of basal and increased dosage of transcription factor SF-1 in the H295R human adrenocortical tumor cell line. 4 samples: input DNA in basal SF-1 expression conditions - FAIRE-seq in basal SF-1 expression conditions - input DNA in SF-1 overexpression conditions - FAIRE-seq in SF-1 overexpression conditions
2013-08-01 | E-GEOD-44221 | biostudies-arrayexpress
Project description:The goal of this study was to identify genomic binding sites of the NRSF/REST transcription factor under conditions of basal and increased SF-1 dosage in the H295R human adrenocortical tumor cell line. 4 samples: input DNA (2 replicates) - NRSF/REST ChIP basal SF-1 dosage - NRSF/REST ChIP increased SF-1 dosage
2013-08-01 | E-GEOD-49014 | biostudies-arrayexpress
Project description:Macrophages have plasticity to adapt microenvironment. In joint tissue, synovial macrophages (SM) and synovial fibroblasts (SF) are maintained in the homeostasis. In Rheumatoid arthritis, crosstalk between SM and SF via inflammatory response induce abnormal activation in respective cells and contribute to disease progression. However, the activation mechanisms in SM which are encouraged by SF are largely unclear. Here, we demonstrated metabolic reprogramming and immunological activation in SM by secretary stimulations from SF using primary culture synovial cell derived from arthritis model mice. To analyze interaction between SM and SF, primary culture of murine synovial cells was performed, respectively. RNA-seq analysis showed SF express abundant secretion-related gene. Thus, we investigated whether conditioned medium from SF (SF-CM) affects biological activity in SM. As the results, SF-CM condition induced both glycolysis and mitochondrial respiration to SM with increased uptake of glucose and glutamine at least, accompanied with cell survival. In addition, several inflammation markers were also upregulated in SM by SF-CM condition. Taken together, these results suggest that metabolic reprogramming were induced in SM by secretory stimulations from SF, followed by activated inflammatory response and long-live. These indicate that such phenotypes of SM may contribute to chronic inflammation in Rheumatoid arthritis
2020-12-09 | GSE142607 | GEO
Project description:SF-1, a transcription factor belonging to the nuclear receptor superfamily, has a pivotal role for adrenogonadal development in humans and mice. A constant feature of childhood adrenocortical tumors (ACT) is SF-1 amplification and overexpression. Using an inducible cellular system, here we show that SF-1 overexpression increases human adrenocortical cell proliferation through opposing effects on cell cycle and apoptosis. SF-1 overexpression also selectively modulates steroidogenesis, reducing cortisol and aldosterone secretion. We identified a novel pro-apoptotic factor for adrenocortical cells, NOV/CCN3, whose levels are significantly reduced by SF-1 overexpression in human adrenocortical cells and are also reduced in primary adrenal tumors. Moreover, Sf-1 overexpression triggers adrenocortical hyperplasia and tumor formation in mice. These tumors express gonadal markers and activated Stat3. Our studies reveal the critical role of SF-1 gene dosage for adrenocortical tumorigenesis and constitute a rationale for the development of drugs targeting SF-1 transcriptional activity for ACT therapy. Keywords: differential expression, transcription factor
2007-01-01 | GSE5911 | GEO
Project description:SF-1, a transcription factor belonging to the nuclear receptor superfamily, has a pivotal role for adrenogonadal development in humans and mice. A constant feature of childhood adrenocortical tumors (ACT) is SF-1 amplification and overexpression. Using an inducible cellular system, here we show that SF-1 overexpression increases human adrenocortical cell proliferation through opposing effects on cell cycle and apoptosis. SF-1 overexpression also selectively modulates steroidogenesis, reducing cortisol and aldosterone secretion. We identified a novel pro-apoptotic factor for adrenocortical cells, NOV/CCN3, whose levels are significantly reduced by SF-1 overexpression in human adrenocortical cells and are also reduced in primary adrenal tumors. Moreover, Sf-1 overexpression triggers adrenocortical hyperplasia and tumor formation in mice. These tumors express gonadal markers and activated Stat3. Our studies reveal the critical role of SF-1 gene dosage for adrenocortical tumorigenesis and constitute a rationale for the development of drugs targeting SF-1 transcriptional activity for ACT therapy. Keywords: comparative gene expression
2007-01-01 | GSE5912 | GEO
Project description:Various forms of chronic arthritis like osteoarthritis (OA) or rheumatoid arthritis (RA) are major causes of disability and represent a global burden on health care systems. Inter- and intraindividual differences in the phenotype of arthritis often prevent early diagnosis and effective treatment. Previously, we suggested that site-specific differences in the joint stroma influence the development and the outcome of arthritis and showed that the long non-coding RNA HOTAIR is expressed exclusively in synovial fibroblasts (SF) of lower joints. Here, we further analysed the function of HOTAIR in SF and in arthritis development. We show that joint-specific HOTAIR expression in SF is stronlgy imprinted in the chromatin landscape of SF by epigenetic mechanisms. Nevertheless, HOTAIR expression in knee SF was downregulated by inflammatory cytokines. Accordingly, HOTAIR was more expressed in OA tissues than in RA tissues. Downregulation of HOTAIR regulated relevant arthritis pathways by epigenetic and transcriptional mechanisms and modified the migratory function of SF, decreased SF mediated osteoclastogenesis, and increased the attraction of B cells by SF. We propose that HOTAIR downregulation in inflammation epigenetically regulates important pathways and functions in SF, and thus modulates the phenotype of arthritis in lower extremity joints.
2023-01-01 | GSE185440 | GEO
Project description:The nuclear receptor steroidogenic factor-1 (SF-1, NR5A1) is a key regulator of adrenal and gonadal biology. We aimed to identify a novel subset of SF-1 target genes in the adrenal by performing ChIP-on-chip in NCI-H295R human adrenocortical cells using promoter tiling arrays. Analysis of ChIP-on-chip experiments with CisGenome identified 738 SF-1-binding regions that met criteria of an MA score more than 3.5 mean ± S.D. and a false discovery rate of <5%. Subsequent analysis focused on those regions that were located between 10 kb upstream and 3 kb downstream of the TSS of known genes, in keeping with the design of the Human Promoter 1.0R arrays. Using this approach, binding regions were annotated to 445 gene loci. The supplementary bed file contains all 946 SF-1 binding sites identified by analysis with CisGenome using standard settings (MA>3.0)
2010-12-17 | GSE26144 | GEO
Project description:SF-1 is a nuclear receptor transcription factor playing a key role in adrenogonadal development and in adrenocortical tumorigenesis when overexpressed. NRSF/REST is a transcriptional repressor that represses expression of neuronal genes in non-neural tissues. Some data suggest that SF-1 and NRSF/REST can functionally interact in adrenocortical cancer cells. We studied gene expression profiles using Affymetrix microarrays in the H295R/TR SF-1 adrenocortical cancer cell line. In this cell line, SF-1 expression can be increased in a doxycycline-dependent manner (Mol. Endocrinol. 21: 2968–2987, 2007). The effects of a control siRNA and sRNAs specific for SF-1 and for NRSF/REST (in basal or increased SF-1 expression conditions) on gene expression were measured.
2013-08-01 | GSE43033 | GEO