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accession-icon GSE11686
Unique Transcriptional Profile in Wrist Muscles From Cerebral Palsy Patients
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Cerebral palsy is caused be an upper motor neuron lesion which casues spasticity as well as secondary effects on muscle . Muscle from cerebral palsy patients is has been shown to be smaller, with more ECM and longer sarcomere lengths

Publication Title

Novel transcriptional profile in wrist muscles from cerebral palsy patients.

Sample Metadata Fields

Sex, Age

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accession-icon SRP019968
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA sequencing data for four cell lines representing different stages during malignant transformation.

Publication Title

Majority of differentially expressed genes are down-regulated during malignant transformation in a four-stage model.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE59337
Malignant-like transformation of normal stem and progenitor cells by myeloid leukemia
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

It has long been known that leukemic cells disrupt normal patterns of blood cell formation, but little is understood about mechanisms. It has generally been assumed that normal hematopoietic stem and progenitor cells (HSPC) are simply out-competed for space by malignant cells. We designed a strategy to determine if leukemic cells alter intrinsic properties and functions of normal HSPCs. Chimeric mice were generated by transplantation of normal marrow and marrow from an inducible transgenic model of chronic myelogenous leukemia (CML). With induction of CML, the composition of the marrow changed dramatically, and normal HSPCs divided more readily and lost their ability to produce lymphocytes. In contrast, only modest changes were recorded in numbers of normal hematopoietic stem cells (HSCs). However, these stem cells were not unscathed, and had reduced reconstitution and self-renewal potential upon transplantation. Interestingly, the normal bystander cells acquired gene expression patterns resembling their neighboring malignant counterparts. This suggested that much of the leukemia signature is mediated by extrinsic factors in the environment.

Publication Title

Treatment of chronic myelogenous leukemia by blocking cytokine alterations found in normal stem and progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP029738
DNA Topoisomerase 1a Promotes RNA-directed DNA Methylation and Histone Lysine 9 Dimethylation at Transposable Elements in Arabidopsis [RNA-Seq]
  • organism-icon Arabidopsis thaliana
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-directed DNA methylation (RdDM) is a transcriptional silencing mechanism mediated by small and long noncoding RNAs produced by the plant-specific RNA polymerases Pol IV and Pol V, respectively. Through a chemical genetics screen with a luciferase-based DNA methylation reporter, LUCL, we found that camptothecin, a compound with anti-cancer properties that targets DNA topoisomerase 1a (TOP1a) was able to de-repress LUCL by reducing its DNA methylation and H3K9 dimethylation (H3K9me2) levels. Further studies with Arabidopsis top1a mutants showed that TOP1a promotes RdDM by facilitating the production of Pol V-dependent long non-coding RNAs, AGONAUTE4 recruitment and H3K9me2 deposition at transposable elements (TEs). Overall design: 5 small RNA libraries were sequenced

Publication Title

DNA topoisomerase 1α promotes transcriptional silencing of transposable elements through DNA methylation and histone lysine 9 dimethylation in Arabidopsis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP062428
Temporal transcriptomics suggest that twin-peaking genes reset the clock
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The mammalian suprachiasmatic nucleus (SCN) drives daily rhythmic behavior and physiology, yet a detailed understanding of its coordinated transcriptional programmes is lacking. To reveal the true nature of circadian variation in the mammalian SCN transcriptome we combined laser-capture microdissection (LCM) and RNA-Seq over a 24-hour light / dark cycle. We show that 7-times more genes exhibited a classic sinusoidal expression signature than previously observed in the SCN. Another group of 766 genes unexpectedly peaked twice, near both the start and end of the dark phase; this twin-peaking group is significantly enriched for synaptic transmission genes that are crucial for light-induced phase-shifting of the circadian clock. 342 intergenic non-coding RNAs, together with novel exons of annotated protein-coding genes, including Cry1, also show specific circadian expression variation. Overall, our data provide an important chronobiological resource (www.wgpembroke.com/shiny/SCNseq/) and allow us to propose that transcriptional timing in the SCN is gating clock resetting mechanisms. Overall design: Pooled dissected tissue of the suprachiasmatic nucleus from five adult male mice provided one of three replicates for each of six timepoints over a 12:12 light/dark (LD) cycle (ZT2, 6, 10, 14, 18 and 22). Each biological replicate was sequenced over 3 seperate lanes using Illumina HiSeq.

Publication Title

Temporal transcriptomics suggest that twin-peaking genes reset the clock.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE25620
Gene profile analysis of sorted Sca1+/cKit- BMCs obtain from mice bearing instigator, non-instigator and Matrigel
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Sca1+/cKit hematopoietic BMCs of hosts bearing instigating tumors (BPLER) promote the growth of responding (HMLER-HR) tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from mice bearing Non-instigating tumors lack this ability

Publication Title

Human tumors instigate granulin-expressing hematopoietic cells that promote malignancy by activating stromal fibroblasts in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE25619
Gene expression profiles of granulin- and control-treated normal human mammary fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To examine the effects of recombinant granulin on human mammary stromal fibroblasts, we cultured normal human mammary fibroblasts in the presence of recombinant human granulin (1ug/ml) or PBS every 24h for 6 days.

Publication Title

Human tumors instigate granulin-expressing hematopoietic cells that promote malignancy by activating stromal fibroblasts in mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP089712
RNA Sequencing of mouse Purkinje cells across postnatal development
  • organism-icon Mus musculus
  • sample-icon 86 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We analyzed Purkinje cell transcriptome dynamics in the developing mouse cerebellum during the first three postnatal weeks, a key developmental period equivalent to the third trimester in human cerebellar development. Our study represents the first detailed analysis of developmental Purkinje cell transcriptomes and provides a valuable dataset for gene network analyses and biological questions on genes implicated in cerebellar and Purkinje cell development. Overall design: Laser capture microdissection was employed to obtain a highly enriched population of cerebellar Purkinje cells. Deep sequencing was performed on RNA isolated from 1000 Purkinje cells at five developmental timepoints (postnatal days P0, P4, P8, P14 and P21) in triplicate.

Publication Title

A gene expression signature in developing Purkinje cells predicts autism and intellectual disability co-morbidity status.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE38333
Genome-wide effects of Pbcas4 knockdown
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We tested the effect iof Pbcas4 knockdown using a specific shRNA on the expression of genes sharing miRNA binding sites in mouse N2A cells.

Publication Title

Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP028399
Transcription Start Site analysis of Mouse Ter119+ erythroid cells
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcription Start Site analysis in Mouse Ter119+ erythroid cells Overall design: Strand Specific Paired end NanoCage analysis of Total RNA from Mouse Ter119+ erythroid cells

Publication Title

Chromatin signatures at transcriptional start sites separate two equally populated yet distinct classes of intergenic long noncoding RNAs.

Sample Metadata Fields

Cell line, 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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