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accession-icon GSE28095
Genetic perturbations direct the development of distinct brain tumor types from postnatal neural stem/progenitor cells
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Primary brain tumors are classified and treated based on their histological features, however the factors which specify these tumor types remain largely unknown. We demonstrate that the over-expression of HRAS (V12) and MYC alone or in combination directs the development of glioma, CNS PNET, and atypical teratoid/rhabdoid (AT/RT)-like tumors from postnatal murine p53-deficient neural stem/progenitor cells.

Publication Title

Definition of genetic events directing the development of distinct types of brain tumors from postnatal neural stem/progenitor cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE70451
Genes differentially expressed between Bmi1-overexpressing and empty vector control neural stem/progenitor cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neural stem/progenitor cells were isolated from the lateral ventricle wall of 4-6 week-old CD1 mice and grown as neurospheres under low density culture conditions. Test cells were transduced with bicistronic retroviral constructs for the over-expression of Bmi1 together with eGFP, and control cells were transduced with an empty vector construct expressing eGFP only. To identify genes, which are regulated by BMI1 in neural stem/progenitor cells, the gene expression profiles of neurosphere cells over-expressing Bmi1 were compared empty vector control cells using Affymetrix Gene mouse ST1.0 arrays

Publication Title

The putative tumor suppressor gene EphA7 is a novel BMI-1 target.

Sample Metadata Fields

Specimen part

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accession-icon GSE57511
Gene expression profile of Dicer knockout in mouse DP thymocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The RNase III enzyme dicer is essential for the processing of microRNAs (miRNAs) and small interfering RNAs (siRNAs) from double-stranded RNA precursors. miRNAs and siRNAs regulate chromatin structure, gene transcription, mRNA stability and translation in a wide range of organisms. To provide a model system to explore the role of dicer-generated RNAs in the differentiation of mammalian cells in vivo, we have generated a conditional dicer allele. Deletion of dicer at an early stage of T cell development compromised the survival of lineage cells, while the numbers of -expressing thymocytes were not affected. In developing thymocytes, dicer was not required for the maintenance of transcriptional silencing at pericentromeric satellite sequences (constitutive heterochromatin), the maintenance of cytosine DNA methylation and X chromosome inactivation in female cells (facultative heterochromatin) and the stable shutdown of a developmentally regulated gene (developmentally regulated gene silencing). Most remarkably, given that one-third of mammalian mRNAs are putative miRNA targets, dicer appears to be dispensable for CD4/8 lineage commitment, a process where epigenetic regulation of lineage choice has been well documented. Thus, although dicer appears critical for the development of the early embryo, it may have limited impact on the implementation of lineage-specific gene expression programs.

Publication Title

microRNAs regulate cell-to-cell variability of endogenous target gene expression in developing mouse thymocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP049021
T-bet recruits P-TEFb to super-enhancers to regulate T helper cell differentiation (RNA-Seq)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The transcription factor T-bet induces differentiation of CD4+ T cells into the Th1 lineage and also allows for a degree of functional plasticity. Here, we show that T-bet acts through super-enhancers to recruit the elongation factor P-TEFb. Th1-specific genes are poised for activation in Th2 cells and P-TEFb recruitment activates transcriptional elongation. T-bet also induces extensive P-TEFb binding at super-enhancers, where it acts to stimulate enhancer RNA transcription. P-TEFb inhibition selectively blocks activation of lineage-specific genes and reverses Th1-associated retinitis pathology. T-bet-mediated recruitment of P-TEFb to super-enhancers at otherwise poised genes provides a model for how lineage-specifying factors promote differentiation towards specific cell fates whilst maintaining a degree of functional plasticity. Overall design: Strand-specific total and poly-A+ RNA-Seq in Th1 and Th2 cells from two independent donors

Publication Title

T-bet Activates Th1 Genes through Mediator and the Super Elongation Complex.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP071700
Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. Overall design: HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturer’s protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.

Publication Title

Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE77153
Expression data from VND7 induction line
  • organism-icon Arabidopsis thaliana
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Plants typically contain two different types of cell walls: a primary wall that is being deposited around all growing cells, and a secondary wall that is produced in cells with specialized functions once they have ceased to grow. In Arabidopsis, VND7 is a transcription factor that is sufficient to activate secondary cell wall synthesis. To artificially turn on the secondary cell wall synthesis, VND7 was fused to the activation domain of the herpes virus VP16 protein and the glucocorticoid receptor (GR) domain. Thus, the transgenic plants harbouring the constructs can then be treated with dexamethasone (DEX), a glucocorticoid derivative, to induce the secondary cell wall formation.

Publication Title

A Transcriptional and Metabolic Framework for Secondary Wall Formation in Arabidopsis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE148414
Eye-antenna early L3 disc expression profiling in combinations of COX7a-LoF, ATF4-LoF and Notch-GoF
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression in larval, early third instar eye-antenna discs was assessed to reveal an ATF4 contribution to target gene induction following COX7a knockdown. As hypothesised, these COX7a-RNAi induced target genes require the transcription factor ATF4 for induction, irrespective of concomitant Notch pathway activation through Delta over-expression.

Publication Title

ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23066
Comparative gene expression analysis of mesenchymal stem cells (MSC) derived from non-small cell lung cancer (NSCLC) and corresponding normal lung tissue (NLT)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The stromal microenvironment plays a vital role in cancer initiation and progression. We performed a comparative expression profiling of pulmonary MSC derived from NSCLC and corresponding normal lung tissue of 5 newly diagnosed patients. The analysis indicated variable expression of genes involved in DNA repair, apoptosis, proliferation or angiogenesis between NSCLC-MSC and NLT-MSC.

Publication Title

Mesenchymal stem cells in non-small cell lung cancer--different from others? Insights from comparative molecular and functional analyses.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE148407
Eye-antenna early L3 disc expression profiling in COX7a-LoF and Notch-GoF
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression in larval, early third instar eye-antenna discs was assesed in genotypes with Notch Gain-of-Function (UAS-Delta or UAS-Notch[intra2]) over-expression or mitochondrial COX7a Loss-of-function (UAS-COX7a-RNAi) or a combination of both (UAS-Delta, UAS-COX7a-RNAi). The analysis revealed that, despite a strong genetic interaction between Notch pathway activation and knockdown of COX7a, no transcriptional cooperation or synergy was detectable in early L3 eye-antenna discs. Rather, COX7a knockdown induced a unique transcriptional signature, which further experiments revealed to be mediated by the transcription factor ATF4.

Publication Title

ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.

Sample Metadata Fields

No sample metadata fields

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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

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)

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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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