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accession-icon GSE59983
Gene expression profiling of primary human retinoblastoma
  • organism-icon Homo sapiens
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Background

Publication Title

Loss of photoreceptorness and gain of genomic alterations in retinoblastoma reveal tumor progression.

Sample Metadata Fields

Specimen part

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accession-icon SRP058046
Genome-wide maps of nuclear lamina interactions in single human cells (CEL-seq)
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaHiSeq2500

Description

Mammalian interphase chromosomes interact with the nuclear lamina (NL) through hundreds of large Lamina Associated Domains (LADs). We report a method to map NL contacts genome-wide in single human cells. Analysis of ~400 maps reveals a core architecture of gene-poor LADs that contact the NL with high cell-to-cell consistency, interspersed by LADs with more variable NL interactions. The variable contacts are more sensitive to a change in genome ploidy than the consistent contacts. Single-cell maps indicate that NL contacts involve multivalent interactions over hundreds of kilobases. Moreover, we observe extensive intra-chromosomal coordination of NL contacts, even over tens of megabases. Such coordinated loci exhibit preferential interactions as detected by Hi-C. Finally, single-cell gene expression and chromatin accessibility analysis shows that loci with consistent NL contacts are expressed at lower levels and are more consistently inaccessible than loci with lower contact frequencies. These results highlight fundamental principles of single cell chromatin organization. Overall design: In this dataset, single-cell mRNA sequencing results from 96 single KBM7 cells have been deposited

Publication Title

Genome-wide maps of nuclear lamina interactions in single human cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE96610
Gene expression data in aortic tissue from rats with experimental preeclampsia, healthy pregnancy and non pregnant rats
  • organism-icon Rattus norvegicus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

Normal pregnancy requires adaptations of the maternal vasculature. During preeclampsia these adjustments are not well established, resulting in maternal hypertension and proteinuria. The effects of preeclampsia on the maternal vasculature are not yet fully understood. We aimed to identify gene expression differences in the aorta between non pregnant, healthy pregnant, and experimental preeclamptic rats using a genome wide approach.

Publication Title

Experimental preeclampsia in rats affects vascular gene expression patterns.

Sample Metadata Fields

Specimen part

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accession-icon E-MTAB-2853
Wuschel Related Homeobox 5 (WOX5) induced overexpression in seedling roots of Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

WOX5 maintains columella stem cells in the Arabidopsis root and prevents their differentiation. In order to understand the molecular mode of WOX5 action the genes differentially expressed by WOX5 inducible over-expression were determined by analysis of microarray hybridizations. Seedlings transformed with a dexamethasone inducible WOX5 construct were induced for one or four hours with dexamethasone or a mock solution. Other seedlings were treated one hour with cycloheximide ( a protein synthesis inhibitor to reduce secondary transcriptional effects after WOX5 activation) and either dexamethasone or a mock solution. Root tips were harvested, RNA extracted, and the RNA samples prepared for hybridization to Affymetrix microarrays. Potential target genes of WOX5 were further analyzed by transcriptional markers, qPCR and EMSA (electrophoretic mobility shift assay).

Publication Title

Organizer-Derived WOX5 Signal Maintains Root Columella Stem Cells through Chromatin-Mediated Repression of CDF4 Expression.

Sample Metadata Fields

Specimen part, Compound, Time

View Samples
accession-icon SRP066947
Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Background. Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). The nuclear lamina (NL) is an important contributor to genome organization and has been involved in cellular senescence and organismal aging. It interacts with multiple regions of the genome called lamina-associated domains (LADs). Some LADs are cell type-specific, while others are conserved between cell types and are referred to as constitutive LADs. Here, we used DamID to investigate the changes in genome-NL interactions in a model of OIS triggered by the expression of the BRAFV600E oncogene.Results. We found that OIS cells lose most of their constitutive LADs (cLADS), suggesting the loss of a specific mechanism that targets cLADs to the NL. In addition, multiple genes relocated to the NL. Unexpectedly, they were not repressed, implying the abrogation of the repressive activity of the NL during OIS. Finally, OIS cells displayed an increased association of telomeres with the NL.Conclusions. Our study reveals that senescent cells acquire a new type of LAD organization and suggest the existence of as yet unknown mechanisms that tether cLADs to the NL and repress gene expression at the NL.

Publication Title

Massive reshaping of genome-nuclear lamina interactions during oncogene-induced senescence.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon SRP170939
Antagonizing increased miR-135a levels at the chronic stage of experimental TLE reduces spontaneous recurrent seizures
  • organism-icon Mus musculus
  • sample-icon 168 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Increased miR-135a levels are observed in human patients with temporal lobe Epilepsy (TLE) and in experimental animal models. Upon targeting the increased miR-135a levels in vivo using antagomirs in kainic acid induced status epilepticus mouse model of TLE, we observed a strong reduction of spontaneous recurrent seizures. To understand this further and to find target mRNAs that potentially mediate the seizure suppressive function of miR-135a, we performed immunoprecipitation using biotin tagged miRNA mimics, followed by RNAsequencing (RNAseq). We found several novel neuronal targets of miRNA-135a and identified Mef2a as a key target in this study. Here we report the total RNAseq data. Overall design: N2A cells were transfected with biotin tagged miRNA mimics for miR-135a and negative control and immunoprecipitations were performed. N = 3 replicates of IP and input samples for each condition were generated and sequenced on illumina platform for total RNA for identification of novel targets of miR-135a.

Publication Title

Antagonizing Increased <i>miR-135a</i> Levels at the Chronic Stage of Experimental TLE Reduces Spontaneous Recurrent Seizures.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE16447
Expression array analysis in patients with neuroaxonal injury in cerebral palsy
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have analysed a family with an autosomal recessive type of tetraplegic cerebral palsy with mental retardation, reduction of cerebral white matter, and atrophy of the cerebellum in an inbred sibship.

Publication Title

Mutation in the AP4M1 gene provides a model for neuroaxonal injury in cerebral palsy.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE63127
Cigarette smoking induces changes in airway epithelial expression of genes associated with monogenic lung disorders
  • organism-icon Homo sapiens
  • sample-icon 202 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Smoking-induced lung disease is one of the most prevalent forms of lung disease but also one of the more diverse. Based on the phenotypic diversity caused by the same environmental stress, we hypothesized that smoking may induce changes in lung cell expression of genes that, with specific variants, are causative of monogenic lung disease, i.e., not that smoking induces a phenocopy of a genetic disease, but smoking may subtly modify the expression of genes known to be associated with genetic disorders with distinct lung disease phenotypes. To assess this hypothesis, and based on the knowledge that most smoking-related disease phenotypes start in the small airway epithelium, we asked: are the genes associated with the monogenic lung disorders expressed in the small airway epithelium, and if so, does smoking alter the expression of these genes? To accomplish this, we examined small airway epithelium expression of 92 genes known to be associated with 17 monogenic lung disorders in 230 samples of small airway epithelium (SAE) obtained from healthy nonsmokers and healthy smokers without any clinical evidence of disease. Of the 86 monogenic disorder-related genes we found expressed in the SAE, strikingly, 37 were significantly differentially expressed in normal smokers compared to normal nonsmokers (p<0.05, Benjamini-Hochberg correction for multiple comparisons). The data demonstrates that the effect of smoking on the transcriptome of small airway epithelium includes significantly altered regulation of the genes responsible for known monogenic disorders.

Publication Title

Cigarette Smoking Induces Changes in Airway Epithelial Expression of Genes Associated with Monogenic Lung Disorders.

Sample Metadata Fields

Sex, Age, Race

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accession-icon GSE10730
Analysis of Iron Deficiency in Soybean Leaf Tissue
  • organism-icon Glycine max
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

This study was designed to identify candidate genes associated with iron efficiency in soybeans. Two genotypes, Clark (PI548553) and IsoClark (PI547430), were grown in both iron sufficient (100uM Fe(NO3)3) and iron deficient (50uM Fe(NO3)3) hydroponics conditions. The second trifoliate was harvested for RNA extraction for the microarray experiment. Candidate genes were identified by comparing gene expression profiles within genotypes between the two iron growth conditions.

Publication Title

Integrating microarray analysis and the soybean genome to understand the soybeans iron deficiency response.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE77094
Gene expression profiles of retinoblastoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

In order to identify the gene targets of frequently altered chromosomal regions in retinoblastoma, a meta-analysis of genome-wide copy number alterations studies on primary retinoblastoma tissue and retinoblastoma cell lines was performed. Published studies were complemented by copy number and gene expression analysis on primary and cell line samples of retinoblastoma. This dataset includes the gene expression data of the retinoblastoma cell lines

Publication Title

A Meta-Analysis of Retinoblastoma Copy Numbers Refines the List of Possible Driver Genes Involved in Tumor Progression.

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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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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