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SRP119557
Homo sapiens
24 Downloadable Samples
Illumina HiSeq 2000
Description
In order to identify and characterize novel human gene expression responses to glucocorticoids, we exposed the human lung adenocarcinoma cell line, A549, to the synthetic glucocorticoid dexamethasone for 1, 3, 5, 7, 9, and 11 hrs in duration as well as to a paired vehicle control, ethanol. We assayed gene expression with RNA-seq and clustered gene expression profiles using an infinite Gaussian process mixture model. Overall design: Time series treatment of human A549 cells with dexamethasone or paired vehicle control.
Publication Title
Clustering gene expression time series data using an infinite Gaussian process mixture model.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Homo sapiens
- 5 Downloadable Samples
- Illumina HiSeq 4000
Description
Purpose: dose response analysis of E2F1 target genes expression in flow-sorted fractions with increasing amounts of fluorescently labled E2F1 Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000. Results: different target genes have different E2F1 activation thresholds. Numerous proliferation-related target genes are induced already by the lowest E2F1-levels. Intermediate E2F1 levels induce cdk inhibitors, which might be responsible for cell cycle arrest. Finally, although some apoptotic E2F1 targets are induced already by low E2F1 levels, many key apoptotic genes require higher E2F1 levels for induction. Conclusions: induction of different cell fates by increasing E2F1 levels might pertain to differential affinities of the targets. Overall design: Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000.
Publication Title
Expression level is a key determinant of E2F1-mediated cell fate.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2000
Description
We examined the transcriptional chagnes modulated by ECBI-11 by perfroming global transcriptome analysis. ZR75 cells were treated with either control or ECBI-11 in the presence of E2 for 48 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that ECBI modulated several genes that are involved in cell cycle, breast cancer signaling, estrogen signaling and apoptosis. Overall design: Total RNA was isolated from the ZR75 cells that were treated with vehicle or ECBI for 48 h. Illumina TruSeq RNA Sample Preparation was performed following manufacturer''s protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.
Publication Title
Estrogen receptor coregulator binding modulators (ERXs) effectively target estrogen receptor positive human breast cancers.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
Our goal was to identify early genetic changes in the development of autoimmune dysfunction. WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice), producing 2X50 paired-end reads using the Illumine HiSeq 2500 platform. Raw reads were provided by Expression Analysis. We identified several genetic signatures within the bulk data including a cytolyic pattern and a novel gene expression pattern indicating a helper-like function. Overall design: WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice).
Publication Title
CD8 Follicular T Cells Promote B Cell Antibody Class Switch in Autoimmune Disease.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 11 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.
Publication Title
The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 60 Downloadable Samples
Affymetrix Rat Genome U34 Array (rgu34a), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Ochratoxin A gene expression profiling in liver and kidney, with time points of exposure from 7 days to 12 motnhs
Publication Title
A toxicogenomics approach to identify new plausible epigenetic mechanisms of ochratoxin a carcinogenicity in rat.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Ewing's Sarcoma cell lines were made resistant to different IGF-1R drugs to investigate mechanisms and pathways modulated by the resistance.
Publication Title
Identification of common and distinctive mechanisms of resistance to different anti-IGF-IR agents in Ewing's sarcoma.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of expression changes in renal collecting duct epithelial cells by adenoviral mediated Krppel like transcription factor 5 (KLF5) overexpression. KLF5 is a key regulator of static and inflammatory stage in renal collecting duct epithelial cells. We thought these results provide insights into downstream genes of KLF5 in renal collecting duct epithelial cells.
Publication Title
Renal collecting duct epithelial cells regulate inflammation in tubulointerstitial damage in mice.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Photoreceptor disorders are collectively known as retinal degeneration (RD), and include retinitis pigmentosa (RP), cone-rod dystrophy and age related macular degeneration (AMD). These disorders are largely genetic in origin; individual mutations in any one of >200 genes cause RD, making mutation specific therapies prohibitively expensive. A better treatment plan, particularly for late stage disease, may involve stem cell transplants into the photoreceptor or ganglion cell layers of the retina. Stem cells from young mouse retinas can be transplanted, and can form photoreceptors in adult retinas. These cells can be grown in tissue culture, but can no longer form photoreceptors. We have used microarrays to investigate differences in gene expression between cultured retinal progenitor cells (RPCs) that have lost photoreceptor potential, postnatal day 1 (pn1) retinas and the postnatal day 5 (pn5) retinas that contain transplantable photoreceptors. We have also compared FACS sorted Rho-eGFP expressing rod photoreceptors from pn5 retinas with Rho-eGFP negative cells from the same retinas. We have identified over 300 genes upregulated in rod photoreceptor development in multiple comparisons, 37 of which have been previously identified as causative of retinal disease when mutated. It is anticipated that this research should bring us closer to growing photoreceptors in culture and therefore better treatments for RD. This dataset is also a resource for those seeking to identify novel retinopathy genes in RD patients.
Publication Title
Gene expression changes during retinal development and rod specification.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 11 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Insulators delimit independent transcriptional domains within genomes by constraining enhancer and silencer action. These transcriptional effects depend upon DNA recognition by insulator binding proteins that recruit partners that protect against inappropriate long range modulation of non-target promoters. Insulator binding proteins are broadly expressed during development, with largely constitutive binding to thousands of genomic sites. Yet, tissue-specific transcriptional changes result from the loss of individual insulator binding proteins. To understand the molecular basis for such effects, we are studying the classic Drosophila insulator protein Suppressor of Hairy-wing [Su(Hw)]. Genetic studies show that loss of this broadly expressed insulator protein prevents oocyte development. To determine the basis for the block in oogenesis, we coupled transcriptional analyses in su(Hw) mutant ovaries with genome-wide definition of Su(Hw) binding in this tissue. These studies identified 71 direct targets of Su(Hw) regulation, with nearly 70% of these genes showing increased RNA accumulation when Su(Hw) is lost. Surprisingly, derepressed Su(Hw) target genes correspond to genes normally highly expressed in neural tissues, suggesting that Su(Hw) has a critical role in silencing neural genes in the ovary. Support for this postulate was obtained by genetic studies. We found that oocyte production was restored in su(Hw) mutant females that carry a deletion of one allele of the elav family RNA binding protein 9 (Rbp9) gene. These su(Hw) null oocytes can be fertilized, with evidence that embryos lacking Su(Hw) show compromised development. Our studies extend the known transcriptional activities of Su(Hw), indicating that Su(Hw) can function as an insulator, activator and repressor, the latter function being essential for oogenesis. These findings highlight that insulator proteins are versatile transcriptional regulatory proteins, suggesting that tissue specific contributions to transcription result from direct regulation of individual genes.
Publication Title
The insulator protein Suppressor of Hairy-wing is an essential transcriptional repressor in the Drosophila ovary.
Sample Metadata Fields
Specimen part
View Samples