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accession-icon SRP055064
Tet1 is a tumor suppressor of hematopoietic maligancy [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and enhanced pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed whole transciptome analysis using RNA-sequencing in purified long-term HSCs and MPPs. These results revealed that genes regulated byTet1 included Histones, DNA repair enzymes and B-lineage specific factors. Overall design: Purified long-term HSCs and MPPs from WT and Tet1 KO mice were used for RNA isolation. RNA was extracted using RNeasy kit (Qiagen) and PolyA selection using oligo-dT beads (Life Technologies) was performed according to the manufacturer's instructions. Libraries were generated as described before, including end-repair, A-tailing, adapter (Illumina Truseq system) ligation and PCR amplification. RNA libraries were then sequenced on the Illumina HiSeq 2000 using 50bp paired-end reads. Transcriptome profiling of LT-HSC and MPP cells in WT and Tet1 KO mice

Publication Title

TET1 is a tumor suppressor of hematopoietic malignancy.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041100
Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [short_hairpins_RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we abrogated the expression of JMJD3 (KDM6B) and UTX (KDM6A) H3K27me3 demethylases in human T-ALL lines and assayed for genome-wide expression changes using RNA sequencing. This piece of data was further integrated to ChIP-Sequencing analysis of H3K27me3 from the same treatment as well as H3K27me3 and JMJD3 genome-wide analysis from treatment of T-ALL lines with the GSKJ4 inhibitor. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role. Overall design: Whole RNA was extracted from 1-5 million T-ALL (lines) cells or primary cells using the RNAeasy kit (Qiagen) according to the manufacturer’s protocol. Poly-A+ (magnetic oligodT-containing beads (Invitrogen)) or Ribominus RNA was used for library preparation. cDNA preparation and strand-specific library construction was performed using the dUTP method. Libraries were sequenced on the Illumina HiSeq 2000 using 50bp single-read method. Differential gene expression analysis was performed for each matched knockdown vs control pairs, separately in each biological or technical replicate in each of two cell lines (CUTLL1, CEM). Three types of comparisons were tested: (a) JMJD3 knockdown vs Renilla, (b) JMJD3 knockdown vs UTX knockdown, and (c) UTX knockdown vs Renilla. Analysis was performed using both DEGseq and Cufflinks packages leading to very similar conclusions.

Publication Title

Contrasting roles of histone 3 lysine 27 demethylases in acute lymphoblastic leukaemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041102
Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [GSKJ4_RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the H3K27me3 demethylase JMJD3 using the GSKJ4 inhibitor and assayed for genome-wide changes in H3K27me3 and JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic knock-down of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role. Overall design: Whole RNA was extracted from 1-5 million primary cells from CUTLL1 human T cell leukemia cells untreated or treated with 2micromolar GSKJ4 using the RNAeasy kit (Qiagen) according to the manufacturer’s protocol. Poly-A+ (magnetic oligodT-containing beads (Invitrogen)) or Ribominus RNA was used for library preparation. cDNA preparation and strand-specific library construction was performed using the dUTP method. Libraries were sequenced on the Illumina HiSeq 2000 using 50bp single-read method. Differential gene expression analysis was performed between knockout vs wild-type background samples. Analysis was performed using DEGseq package leading to very similar conclusions.

Publication Title

Contrasting roles of histone 3 lysine 27 demethylases in acute lymphoblastic leukaemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041101
Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [UTXKO_RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we conduct expression analysis in NOTCH1-IC-induced tumors in Utx wild-type (Utx+/+ or Utx+/Y) and knockout (Utx-/Y) background. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to characterize the hitherto understudied role of Utx as an oncogenic facilitator in leukemia and the contrasting expression signatures between JMJD3 and UTX in this disease. Overall design: Whole RNA was extracted from 1-5 million primary cells from Notch1-IC-expressing (sorted populations of) mouse T-ALL tumors using the RNAeasy kit (Qiagen) according to the manufacturer’s protocol. Poly-A+ (magnetic oligodT-containing beads (Invitrogen)) or Ribominus RNA was used for library preparation. cDNA preparation and strand-specific library construction was performed using the dUTP method. Libraries were sequenced on the Illumina HiSeq 2000 using 50bp single-read method. Differential gene expression analysis was performed between knockout vs wild-type background samples. Analysis was performed using DEGseq package leading to very similar conclusions.

Publication Title

Contrasting roles of histone 3 lysine 27 demethylases in acute lymphoblastic leukaemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE33826
Gene expression in Plasmodium falciparum NF54 and P. falciparum HOX
  • organism-icon Plasmodium falciparum
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

P. falciparum NF54 proliferates under micro-aerophilic conditions in an environment of 3% O2, 4% CO2, 93% N2. This strain was gradually adapted to proliferate under standard tissue culture conditions of 5% CO2/95% air (~19% O2) to generate P. falciparum HOX. We compared global gene expression profiles of the two strains to identify differences, if any.

Publication Title

Model system to define pharmacokinetic requirements for antimalarial drug efficacy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9951
Transcriptome analyses in normal prostate epithelial cells following exposure to low-dose cadmium
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

BACKGROUND: Cadmium is implicated in prostate carcinogenesis, but its oncogenic action remains unclear.

Publication Title

Transcriptome analyses in normal prostate epithelial cells exposed to low-dose cadmium: oncogenic and immunomodulations involving the action of tumor necrosis factor.

Sample Metadata Fields

Sex

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accession-icon GSE58771
Expression data from Arabidopsis thaliana root and piriformaspora indica during log and short term interaction
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Piriformospora indica, an endophytic fungus of Sebacinales, colonizes the roots of many plant species including Arabidopsis thaliana. The symbiotic interaction promotes plant per-formance, growth and resistance/tolerance against abiotic and biotic stress. We demonstrate that exudated compounds from the fungus activate stress and defense responses in the Arabidopsis roots and shoots before the two partners are in physical contact. They induce stomata closure, stimulate reactive oxygen species (ROS) production, stress-related phytohormone accumulation and activate defense and stress genes in the roots and/or shoots. Once a physical contact is established, the stomata re-open, ROS and phytohormone levels decline, and the gene expression pattern indicates a shift from defense to mutualistic interaction.

Publication Title

The interaction of Arabidopsis with Piriformospora indica shifts from initial transient stress induced by fungus-released chemical mediators to a mutualistic interaction after physical contact of the two symbionts.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE55617
Gene expression of liver tissue from Pcyt2 mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Pcyt2 defient mice has metabolic syndrome and insulin resistance. We used microarray to study the gene expression of these mice to

Publication Title

Male-Specific Cardiac Dysfunction in CTP:Phosphoethanolamine Cytidylyltransferase (Pcyt2)-Deficient Mice.

Sample Metadata Fields

Specimen part

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accession-icon SRP131270
Transcription start site analysis reveals widespread divergent transcription in D. melanogaster and core promoter-encoded enhancer activities
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Sequencing of 5'' ends of RNA molecules from control and exosome-depleted S2 cells. Overall design: CAGE library construction from RNA extracted from control and exosome-depleted cells.

Publication Title

Transcription start site analysis reveals widespread divergent transcription in D. melanogaster and core promoter-encoded enhancer activities.

Sample Metadata Fields

Subject

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accession-icon GSE29670
Polymicrobial periodontal pathogens transcriptomes in calvarial bone and soft tissue
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The objectives of this investigation were to examine changes in the host transcriptional profiles during a polymicrobial periodontal pathogens Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia infection using a murine calvarial model of inflammation and bone resorption. P. gingivalis FDC 381, T. denticola ATCC 35404, and T. forsythia ATCC 43037 was injected into the subcutaneous soft tissue over the calvaria of BALB/c mice for 3 days, after which the soft tissues and calvarial bones were excised. RNA was isolated from infected soft tissues and calvarial bones and analyzed for transcript profiles using Murine GeneChip MG-MOE430A Affymetrix arrays to provide a molecular profile of the events that occur following infection of these tissues.

Publication Title

Polymicrobial periodontal pathogen transcriptomes in calvarial bone and soft tissue.

Sample Metadata Fields

Age, Specimen part

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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