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GSE40493
Mus musculus
8 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
gene expression data from wild-type and Bcl6-/- regulatory T cells
Publication Title
Bcl6 controls the Th2 inflammatory activity of regulatory T cells by repressing Gata3 function.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 30 Downloadable Samples
IlluminaHiSeq2000
Description
Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) – the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation. Overall design: RNA-seq profiles of prostate cancer cell lines to understand gene expression associated with enzalutamide treatment
Publication Title
Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
LSD1 activates a lethal prostate cancer gene network independently of its demethylase function.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Rigosertib treatment of head and neck squamous cell cancer
Publication Title
The dual pathway inhibitor rigosertib is effective in direct patient tumor xenografts of head and neck squamous cell carcinomas.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Circadian profiling of total RNA collected from wildtype and NPY KO murine liver. Liver RNA collected every 4 hours in a 12hr light:12hr dark cycle.
Publication Title
Neural clocks and Neuropeptide F/Y regulate circadian gene expression in a peripheral metabolic tissue.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 15 Downloadable Samples
- NextSeq 500
Description
The spliceosome is a dynamic RNA-protein complex that executes pre-mRNA splicing and is composed of five core small nuclear ribonucleoprotein particles (U1, U2, U4/5/6 snRNP) and >150 additional proteins specific for each snRNP. We report a circadian role for Pre-mRNA Processing factor 4 (PRP4), a conserved component of the spliceosomal U4/U6.U5 triple small nuclear ribonucleoprotein (tri-snRNP) complex. We broadly hypothesized that downregulation of prp4 led to the aberrant splicing of one or many of the core clock transcripts. To identify these splicing events in an unbiased way, we performed RNA-Sequencing (RNA-Seq) analysis. We reasoned that we could have a more targeted approach if we could zoom in on the overlapping splicing changes that would be driven by the knockdown of at least two different tri-snRNP components. Because the pan-neuronal knockdown of all tri-snRNP components tested in our study led to lethality, we decided to utilize an alternative broad driver. For that purpose, we selected a strong eye-specific Glass Multiple Promoter driver (GMR-Gal4). Because most of the signal from head lysates comes directly from the eye tissue and because the core splicing factors are ubiquitously expressed, GMR-specific downregulation of prp4 and prp8 promised to be a viable alternative to the pan-neuronal knockdown. We examined changes in both the total transcript levels and splicing events upon prp4 knockdown in the eye. The overall gene expression seemed to be dramatically influenced by prp4 downregulation (433 DOWN, 310 UP at FDR < 0.05). Despite the fact that PRP4 is a component of the core spliceosome that is required for constitutive exon splicing, we did not detect dramatic effects on global splicing. Only 45 genes exhibited differential alternate splicing upon prp4 downregulation at FDR < 0.05). Overall design: 3 samples with 5 replicates each were analyzed using Illumina Next-Generation Sequencing (NextSeq 500).
Publication Title
Spliceosome factors target timeless (<i>tim</i>) mRNA to control clock protein accumulation and circadian behavior in Drosophila.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In skeletal muscle differentiation, muscle-specific genes are regulated by two groups of transcription factors, the MyoD and MEF2 families, which work together to drive the differentiation process. Here we show that ERK5 regulates muscle cell fusion through Klf transcription factors. The inhibition of ERK5 activity suppresses muscle cell fusion with minimal effects on the expression of MyoD, MEF2, and their target genes. Promoter analysis coupled to microarray assay reveals that Klf-binding motifs are highly enriched in the promoter regions of ERK5-dependent upregulated genes. Remarkably, Klf2 and Klf4 expression are also upregulated during differentiation in an ERK5-dependent manner, and knockdown of Klf2 or Klf4 specifically suppresses muscle cell fusion. Moreover, we show that the Sp1 transcription factor links ERK5 to Klf2/4, and that nephronectin, a Klf transcriptional target, is involved in muscle cell fusion. Therefore, an ERK5/Sp1/Klf module plays a key role in the fusion process during skeletal muscle differentiation.
Publication Title
ERK5 regulates muscle cell fusion through Klf transcription factors.
Sample Metadata Fields
Cell line, Time
View Samples- Mus musculus
- 138 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Note: non-normalized values and associated raw data cannot be located by the submitter
Publication Title
Maternal nutrition induces pervasive gene expression changes but no detectable DNA methylation differences in the liver of adult offspring.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 40 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
The aim of this study is to characterize transcriptional changes induced by maternal diet in several adult tissues and to test whether differences in DNA methylation or microRNA expression could explain these changes.
Publication Title
Maternal nutrition induces pervasive gene expression changes but no detectable DNA methylation differences in the liver of adult offspring.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 40 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
The aim of this study is to characterize transcriptional changes induced by maternal diet in several adult tissues and to test whether differences in DNA methylation or microRNA expression could explain these changes.
Publication Title
Maternal nutrition induces pervasive gene expression changes but no detectable DNA methylation differences in the liver of adult offspring.
Sample Metadata Fields
Sex, Specimen part
View Samples