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accession-icon E-MEXP-157
Transcription profiling of SBH/y rats vs SBN/y rats under basal conditions and after salt loading
  • organism-icon Rattus norvegicus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a), Affymetrix Rat Expression 230B Array (rae230b)

Description

Gene expression was studied in whole kidneys in a 2 x 2 design. SBH/y were contrasted with SBN/y under basal conditions and after salt loading. Thus, four groups were studied altogether. Five rats were used in each group. Altogether, 20 animals were used, and each animal was studied separately. Gene expression was done in kidney. Differential gene expression was measured 4 weeks after initiation of salt loading. At that time point hypertension invariably evolves fully in SBH/y but not in SBN/y.<br></br><br></br>Affymetrix CHP files are available on request from arrayexpress@ebi.ac.uk

Publication Title

Identification of hypertension-related genes through an integrated genomic-transcriptomic approach.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject, Compound

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accession-icon GSE6573
Dysregulation of the circulating and tissue-based renin-angiotensin system in preeclampsia
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps.

Publication Title

Dysregulation of the circulating and tissue-based renin-angiotensin system in preeclampsia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP109805
A map of human circular RNAs in clinically-relevant tissues
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Cellular circular RNAs (circRNAs) are generated by head-to-tail splicing and are present in all multicellular organisms studied so far. Recently, circRNAs have emerged as large class of RNA which can function as post-transcriptional regulators. It has also been shown that many circRNAs are tissue- and stage specifically expressed. Moreover, the unusual stability and expression specificity make circRNAs important candidates for clinical biomarker research. Here, we present a circRNA expression resource of twenty human tissues highly relevant to disease-related research: vascular smooth muscle cells (VSMCs), human umbilical vein (HUVECs), artery endothelial cells (HUAECs), atrium, vena cava, neutrophils, platelets, cerebral cortex, placenta, and samples from mesenchymal stem cell differentiation. In eight different samples from a single donor, we found highly tissue-specific circRNA expression. Circular-to-linear RNA ratios revealed that many circRNAs were higher expressed than their linear host transcripts. Among the 65 validated circRNAs, we noticed potential biomarkers. In adenosine deaminase-deficient, severe combined immunodeficiency (ADA-SCID) patients and in Wiskott-Aldrich-Syndrome (WAS) patients' samples, we found evidence for differential circRNA expression of genes that are involved in the molecular pathogenesis of both phenotypes. Our findings underscore the need to assess circRNAs in mechanisms of human disease. Overall design: To explore circRNA expression patterns in human tissues, we performed rRNA-depleted RNA sequencing and circRNA detection in twenty clinically relevant samples.

Publication Title

A map of human circular RNAs in clinically relevant tissues.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon GSE1557
Terminal heart failure
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats.

Publication Title

Cardiac gene expression profile in rats with terminal heart failure and cachexia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20200
Exon-Level Expression Data from Primary B Cells, Early Proliferating EBV-infected B Cells and Lymphoblastoid Cell Lines
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Eptstein-Barr Virus, an oncogenic herpesvirus, infects and immortalizes human B cells in culture into indefinitely-proliferating LCLs. We examined the gene expression of primary B cells during the process of infection and growth transformation at the exon level to analyze early and late virus-induced changes in expression and exon usage.

Publication Title

An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE24295
Gene expression in epithelial and non-epithelial cells of renal origin
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We aimed to define epithelial-specific genes in the kidney. In the developing mouse kidney at E12.5 epithelial cells are restricted to the ureteric bud, while mesenchymal cells surrounding the ureteric bud are non-epithelial. The mouse renal epithelial cell line mIMCD-3 was used to represent kidney epithelia in vitro. Gene expression was analyzed using Affymetrix microarrays in ureteric bud stalks, ureteric bud tips, and mIMCD-3 cells and compared to metanephric mesenchyme.

Publication Title

The transcription factor grainyhead-like 2 regulates the molecular composition of the epithelial apical junctional complex.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE53225
Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

miR-92 enhances c-Myc induced apoptosis. In the R26MER/MER mouse embryonic fibroblasts (MEFs), a switchable variant of Myc, MycERT2, was knocked into the genomic region downstream of the constitutive Rosa26 promoter, allowing acute activation of c-Myc by 4-OHT-induced nuclear translocation. This in vitro system nicely recapitulates c-Myc-induced apoptosis, as activated MycERT2 induces strong p53-dependent apoptosis in response to serum starvation. Enforced miR-92 expression in three independent R26MER/MER MEF lines significantly enhanced Myc-induced apoptosis.

Publication Title

A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis.

Sample Metadata Fields

Specimen part

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accession-icon GSE108904
Heart tissue expression data from dTGR rats treated with or without BAY 41-8543 and Sprague Dawley control rats
  • organism-icon Rattus norvegicus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.1 ST Array (ragene21st)

Description

We aimed to characterize the complex cardiovascular effects of NOsGC stimulation using NO-independent stimulator BAY 41-8543 in a double transgenic rat (dTGR) model of HFpEF.

Publication Title

Nitric oxide-sensitive guanylyl cyclase stimulation improves experimental heart failure with preserved ejection fraction.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE4774
ruben-affy-mouse-187820
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Dlx homeobox genes have central roles in controlling patterning and differentiation of the brain and craniofacial primordia. In the brain, loss of Dlx function results in defects in the production, migration and differentiation of GABAergic neurons, that can lead to epilepsy. In the branchial arches, loss of Dlx function leads to craniofacial malformations that include trigeminal axon pathfinding defects. To determine how these genes function, we wish to identify the transcriptional circuitry that lies downstream of these transcription factors by comparing gene expression in wild type with Dlx mutant CNS and craniofacial tissues.

Publication Title

Dlx genes pattern mammalian jaw primordium by regulating both lower jaw-specific and upper jaw-specific genetic programs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP149374
RNA sequencing of bone marrow CD34+ hematopoietic stem and progenitor cells from patients with myelodysplastic syndrome and healthy controls
  • organism-icon Homo sapiens
  • sample-icon 765 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

SF3B1, SRSF2 and U2AF1 are the most frequently mutated splicing factor genes in MDS. We have performed a comprehensive analysis to determine the impact of these commonly mutated splicing factors on pre-mRNA splicing in the stem/progenitor cells and in the erythroid and myeloid precursors in splicing factor mutant MDS. Using RNA-seq, we determined the aberrantly spliced genes and dysregulated pathways in bone marrow CD34+ cells of a large group of 82 MDS patients. Splicing factor mutations in MDS result in different mechanistic alterations in splicing and largely affect different genes, but these converged in common dysregulated pathways and cellular processes, including RNA splicing, translation and mitochondrial dysfunction, indicating that these mutations operate through common mechanisms in MDS. Many of these dysregulated pathways and cellular processes can be linked to the known disease pathophysiology and to the phenotypes associated with splicing factor mutations in MDS, whilst several others have not been previously associated with MDS, such as sirtuin signalling. Overall design: RNA-sequencing was performed on bone marrow CD34+ hematopoeitic stem and progenitor cells from patients with myelodysplastic syndrome and healthy controls to identify differential splicing between samples with mutations in the splicing factor SF3B1, SRSF2 or U2AF1 comparative to samples from myelodysplactic syndrome patients without mutations in these splicing factors and healthy controls. Processed data for the CD34+ hematopoeitic stem and progenitor cells are available in the files: CPM_table.txt.gz, Count_table.txt.gz and TPM_table.txt.gz. RNA-sequencing was also performed on monocytic, granulocytic and erythroid precursors from the bone marrow of patients with myelodysplastic syndrome and healthy controls to identify aberrant splicing in samples with mutations in splicing factors SF3B1 and SRSF2 comparative from healthy controls. Processed data for the monocytic, granulocytic and erythroid precursors are available in the files: CPM_table_fractions.txt, Count_table_fractions.txt and TPM_table_fractions.txt.

Publication Title

Impact of spliceosome mutations on RNA splicing in myelodysplasia: dysregulated genes/pathways and clinical associations.

Sample Metadata Fields

Specimen part, Disease, Subject

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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)

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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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