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accession-icon SRP044099
The contribution of cohesin-SA1 to chromatin architecture and gene expression in two murine tissues
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Cohesin, which consists of SMC1, SMC3, Rad21 and either SA1 or SA2, topologically embraces the chromatin fibers to hold sister chromatids together and to stabilize chromatin loops. Increasing evidence indicates that these loops are the organizing principle of higher-order chromatin architecture, which in turn is critical for gene expression. To determine how cohesin contributes to the establishment of tissue-specific transcriptional programs, we compared genome-wide cohesin distribution, gene expression and chromatin architecture in cerebral cortex and pancreas from adult mice. More than one third of cohesin binding sites differ between the two tissues and these are enriched at the regulatory regions of tissue-specific genes. Cohesin colocalizes extensively with the CCCTC-binding factor (CTCF). Cohesin/CTCF sites at active enhancers and promoters contain, at least, cohesin-SA1 whereas either cohesin-SA1 or cohesin-SA2 are present at active promoters independently of CTCF. Analyses of chromatin contacts at the Protocadherin gene cluster and the Regenerating islet-derived (Reg) gene cluster, mostly expressed in brain and pancreas respectively, revealed remarkable differences in the architecture of these loci in the two tissues that correlate with the presence of cohesin. Moreover, we found decreased binding of cohesin and reduced transcription of the Reg genes in the pancreas of SA1 heterozygous mice. Given that Reg proteins are involved in the control of inflammation in pancreas, such reduction may contribute to the increased incidence of pancreatic cancer reported in these animals. Overall design: Examination of the relationship between gene expression, genome wide cohesin distribution and chromatin structure

Publication Title

The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16499
Heart Failure Associated Changes in Alternative Splicing of Sarcomere Genes
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Alternative mRNA splicing is an important mechanism for regulation of gene expression. Changes in gene expression contribute to the pathogenesis of heart failure. However, changes in mRNA splicing have not been systematically examined in heart disease. We hypothesized that mRNA splicing is changed in diseased hearts.

Publication Title

Heart failure-associated changes in RNA splicing of sarcomere genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE141955
Expression data from adult myocardium of ToF-PVR patients undergoing pulmonary valve replacement
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Adult right ventricle from Tetralogy of Fallot patients undergoing pulmonary valve replacement vs right ventricle myocardium from unused donor hearts

Publication Title

Right Ventricle Has Normal Myofilament Function But Shows Perturbations in the Expression of Extracellular Matrix Genes in Patients With Tetralogy of Fallot Undergoing Pulmonary Valve Replacement.

Sample Metadata Fields

Specimen part

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accession-icon GSE55232
Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart
  • organism-icon Homo sapiens
  • sample-icon 129 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE55231
Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart: gene expression
  • organism-icon Homo sapiens
  • sample-icon 129 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

In recent years genome-wide association studies (GWAS) have uncovered numerous chromosomal loci associated with various electrocardiographic traits and cardiac arrhythmia predisposition. A considerable fraction of these loci lie within inter-genic regions. Trait-associated SNPs located in putative regulatory regions likely exert their effect by modulating gene expression. Hence, the key to unraveling the molecular mechanisms underlying cardiac traits is to interrogate variants for association with differential transcript abundance by expression quantitative trait locus (eQTL) analysis. In this study we conducted an eQTL analysis of human heart. To this end, left ventricular mycardium samples from non-diseased human donor hearts were hybridized to Illumina HumanOmniExpress BeadChips for genotyping (n = 129) and Illumina Human HT12 Version 4 BeadChips (n = 129) for transcription profiling.

Publication Title

Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP090469
RNAseq analysis of Rpl13a-snoless and wild type islets
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: To gain further mechanistic insight into phenotypic differences between wild type pancreatic islets and islets with loss of function of 4 Box C/D snoRNAs from the Rpl13a locus (U32a, U33, U34 and U35a). Methods:High quality total RNA (RIN = 8.5) was prepared from hand-picked islets (n = 4 mice/genotype) using TRIZOL reagent, treated with Turbo DNAse (Thermo Fisher), and used to prepare SeqPlex RNAseq libraries (Sigma). Sequencing was performed by the Washington University Genome Technology Access Center using two lanes of Illumina HiSeq 2500, 1x50. Reads were demultiplexed and trimmed, and STAR alignment and quantification analysis was carried out using the Partek Flow platform. Uniquely aligned reads were quantified to identify genes with at least a two-fold change between genotypes with p < 0.05 and FDR step-up of 0.05. Results:We observed 2-fold or greater differences in the expression of only six genes. Conclusions: Our data indicate that loss-of-function of snoRNAs from the Rpl13a locus is associated with modest changes in mRNA abundance. Overall design: Examination of murine pancreatic islet mRNA differential expression between wild type mice and mice with loss-of-function of U32a, U33, U34, and U35a snoRNAs.

Publication Title

Rpl13a small nucleolar RNAs regulate systemic glucose metabolism.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE18732
mRNA expression data from skeletal muscle of type 2 diabetes
  • organism-icon Homo sapiens
  • sample-icon 117 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarray technology to profile mRNA expression in the skeletal muscle of normal (NGT), glucose intolerant (IGT) and type 2 diabetic (DM) subjects. Groups were classified using WHO criteria and, importantly, the DM group were free of anti hypoglycaemic medication for one week prior to biopsy.

Publication Title

Integration of microRNA changes in vivo identifies novel molecular features of muscle insulin resistance in type 2 diabetes.

Sample Metadata Fields

Sex, Age

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accession-icon GSE197751
Cigarette smoke extract disturbs mitochondria-regulated airway epithelial cell responses to pneumococci
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.

Publication Title

Cigarette Smoke Extract Disturbs Mitochondria-Regulated Airway Epithelial Cell Responses to Pneumococci.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE13314
Gene expression profiling of pulmonary MALT lymphoma
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Molecular pathways activated in MALT lymphoma are not well defined.

Publication Title

Gene expression profiling of pulmonary mucosa-associated lymphoid tissue lymphoma identifies new biologic insights with potential diagnostic and therapeutic applications.

Sample Metadata Fields

Sex

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accession-icon GSE20948
The Effect of Hepatitis C Virus Infection on Host Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatitis C Virus is a leading cause of chronic liver disease. The identification and characterisation of key host cellular factors that play a role in the HCV replication cycle is important for the understanding of disease pathogenesis and the identification of novel anti-viral therapeutic targets. Gene expression profiling of HCV infected Huh7 cells by microarray analysis was performed to identify host cellular genes that are transcriptionally regulated by infection. The expression of host genes involved in cellular defence mechanisms (apoptosis, proliferation and anti-oxidant responses), cellular metabolism (lipid and protein metabolism) and intracellular transport (vesicle trafficking and cytoskeleton regulation) was significantly altered by HCV infection. The gene expression patterns identified provide insight into the potential mechanisms that contribute to HCV associated pathogenesis. These include an increase in pro-inflammatory and pro-apoptotic signalling and a decrease in the anti-oxidant response pathways of the infected cell.

Publication Title

Gene expression profiling indicates the roles of host oxidative stress, apoptosis, lipid metabolism, and intracellular transport genes in the replication of hepatitis C virus.

Sample Metadata Fields

Specimen part, Cell line

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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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