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accession-icon GSE23895
Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency.

Publication Title

Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE54011
C. Elegans expression: toxic vs. adequate vs. low selenium
  • organism-icon Caenorhabditis elegans
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Genome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations

Publication Title

Toxic-selenium and low-selenium transcriptomes in Caenorhabditis elegans: toxic selenium up-regulates oxidoreductase and down-regulates cuticle-associated genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP063901
The binding specificity and regulatory effect of WT and redesigned Puf2p [RNA-Seq]
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PUF proteins have become a leading scaffold for designing RNA-binding proteins to contact and control RNAs at will. We analyze the effects of that reengineering across the transcriptome in vivo for the first time. We show, by HITS-CLIP and PAR-CLIP, that S. cerevisiae Puf2p, a non-canonical PUF protein, binds more than 1000 mRNA targets. Puf2p binds multiple UAAU elements, unlike canonical PUF proteins. We also perform CLIP-seq on truncations of Puf2p, showing that its prion domain is dispensable for WT binding. We design a modified Puf2p to bind UAAG rather than UAAU, which allows us to align the protein with the binding site. In vivo, the redesigned protein binds UAAG sites. Its altered specificity redistributes the protein away from 3'UTRs, such that the protein tracks with its sites and binds throughout the mRNA. We use RNA-seq to determine that R1 SNE Puf2p represses a novel RNA network.  Overall design: CLIP-seq was performed in BY4742 S. cerevisiae grown in log phase, and using 2 replicates of TAP-tagged proteins. RNA-seq was performed to determine the regulatory effect of WT or mutant Puf2p, using 4 replicates of the control (no Puf2p), 3 of WT Puf2p and 4 of R1 SNE Puf2p.

Publication Title

Target selection by natural and redesigned PUF proteins.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE41993
Expression data from the reproductive tracts of WT, Hoxa9,10,11, and Hoxd9,10,11 mutant mice
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition, we observed a surprising anti-dogmatic posteriorization of the uterine epithelium.

Publication Title

Recombineering-based dissection of flanking and paralogous Hox gene functions in mouse reproductive tracts.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP017207
RNA-Seq expression data from the reproductive tracts of WT, Hoxa91011, and Hoxd91011 mutant mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition we observed a surprising anti-dogmatic posteriorization of the uterine epithelium. Overall design: Reproductive tracts were collected from WT and Hox mutant mice (n=3/genotype) aged 3-7 months in order to characterize the molecular changes caused by mutation of Hoxa9,10,11 and Hoxd9,10,11. Female mice were staged and collected in diestrus.

Publication Title

Recombineering-based dissection of flanking and paralogous Hox gene functions in mouse reproductive tracts.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE8514
Expression data from normal adrenal gland and aldosterone-producing adenoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The source of aldosterone in 30 to 40 % of patients with primary hyperaldosteronism (PA) is unilateral aldosterone-producing adenoma (APA). The mechanisms causing elevated aldosterone production in APA are unknown. Herein, we examined expression of G-protein coupled receptors (GPCR) in APA and demonstrate that compared to normal adrenals there is a general elevation of certain GPCR in many APA and/or ectopic expression of GPCR in others. RNA samples from normal adrenals (n = 5), APAs (n = 10), and cortisol-producing adenomas (CPAs) (n=13) were used on 15 genomic expression arrays, each of which included 223 GPCR transcripts presented in at least one out of 15 of the independent microarrays. The array results were confirmed using real-time RT-PCR (qPCR). Four GPCR transcripts exhibited a statistically significant increase that was greater than 3-fold compared to normal adrenals, suggesting a general increase in expression compared to normal adrenal glands. Four GPCR transcripts exhibited a greater than 15-fold increase of expression in one or more of the APA samples compared to normal adrenals. qPCR analysis confirmed array data and found the receptors with the highest fold increase in APA expression to be luteinizing hormone receptor (LH-R), serotonin receptor 4 (HTR4), gonadotropin-releasing hormone receptor (GnRHR), glutamate receptor metabotropic 3 (GRM3), endothelin receptor type B-like protein (GPR37), and ACTH receptor (MC2R). There are also sporadic increased expressions of these genes in the CPAs. Together, these findings suggest a potential role of altered GPCR expression in many cases of PA and provide candidate GPCR for further study.

Publication Title

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20676
Genome-wide analysis of adrenocortical cells gene expression after 48 h ACTH treatment
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ACTH is a potent regulator of gene expression in human adrenal cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE20675
Genome-wide analysis of fetal adrenocortical cells gene expression after 48 h ACTH treatment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Analysis of ACTH-regulation on adrenocortical cells at gene expression level. The hypothesis tested in the present study was that ACTH increases chronic cell growth and steroidogenesis in adrenal glands by changing the gene expression profile. Results provide important information on the changes of gene expression of adrenocortical cells after chronic ACTH treatment.

Publication Title

ACTH is a potent regulator of gene expression in human adrenal cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE20669
Genome-wide analysis of adult adrenocortical cells gene expression after 48 h ACTH treatment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Analysis of ACTH-regulation on adrenocortical cells at gene expression level. The hypothesis tested in the present study was that ACTH increases chronic cell growth and steroidogenesis in adrenal glands by changing the gene expression profile. Results provide important information of the response of adrenocortical cells gene expression to chronic ACTH treatment.

Publication Title

ACTH is a potent regulator of gene expression in human adrenal cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE49877
Human intestinal T cell and paired blood transcriptomes
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The intestinal mucosa harbors the largest accumulation of T lymphocytes in the body. While these T cells play an important role in immune homeostasis, they are also implicated in triggering and maintaining pathological intestinal inflammation. In humans they are poorly characterised, and even mouse transcriptomes have been reported for only a few individual cell types, many of which lack direct human equivalents. Using expression microarrays on T cells isolated from ileal biopsies and in silico analysis, we present here an unbiased, transcriptome-wide view of function in T cell subpopulations of the healthy human intestine and delineate signalling pathways that are distinct from those seen in peripheral blood T cells.

Publication Title

Generation of primary human intestinal T cell transcriptomes reveals differential expression at genetic risk loci for immune-mediated disease.

Sample Metadata Fields

Sex, Specimen part

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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