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accession-icon GSE41243
Gene expression from Gaucher Disease iPSc
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Gene expression data obtained from induced pluripotent stem cells derived from wild type fibroblasts (iPSc WT) and from Gaucher Disease type 2 fibroblasts (GD iPSc). Also, gene expression analysis from the initial fibroblasts was made (WT fibroblasts and GD- fibroblasts), as well as gene expression analysis from a human embryonic stem cell line (hES4).

Publication Title

Neuronopathic Gaucher's disease: induced pluripotent stem cells for disease modelling and testing chaperone activity of small compounds.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE52892
SOX11-positive and SOX11-knockdown xenograft derived tumor Gene Expression Profilings
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL). We have recently demonstrated SOX11 tumorigenic potential in vivo by showing a significant reduction on tumor growth of SOX11-knockdown MCL cells in xenograft experiments, confirming the clinical observations that SOX11 may play an important role in the aggressive behavior of MCL (Vegliante et al., 2013). However, the specific mechanisms regulated by SOX11 that promote the oncogenic and rapid tumor growth of aggressive MCL still remain to be elucidated. To further characterize the potential oncogenic mechanisms regulated by SOX11 in MCL, we have analyzed the GEP derived from the xenograft SOX11-positive and knockdown xenograft derived tumors.

Publication Title

SOX11 promotes tumor angiogenesis through transcriptional regulation of PDGFA in mantle cell lymphoma.

Sample Metadata Fields

Specimen part

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accession-icon SRP100068
Differential gene expression in Jagged1 treated human dental pulp cells.
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The present study aimed to determine mRNA expression profilling of indirect immobilized Jagged1 treated human dental pulp cells. Human dental pulp cells were seeded on indirect immobilized Jagged1 surface for 24 h. Cells on hFc immobilized surface was employed as the control. RNA sequencing was performed using NextSeq500, Illumina. Data were processed on FastQC and FastQ Toolkit and subsequently mapped with Homo sapiens hg38 using TopHat2. Mapped data were processed through Cufflink2 and Cuffdiff2. Results demonstrated 1,465 differentially expressed genes in Jagged1 treated cells compared with the control. Enriched pathway analysis revealed that Jagged1 treated cells upregulated genes mainly involved in extracellular matrix organization, disease, and signal transduction categories. However, genes related to cell cycle, DNA replication and DNA repair categories were downregulated. In conclusion, Jagged1 activates Notch signaling and regulates cell cycle pathway in hDPs. Overall design: The mRNA profiles of human dental pulp cells treated with indirect immobilized Jagged1 (10nM) for 24 h was evaluated by next genereation RNA sequencing (NextSeq 500, Illumina) in triplicates. Cells on hFc immobilized surface was used as the control. In some condition, cells were pretreated with a gamma secretase inhibitor (DAPT; 20 uM) for 30 mins prior to Jagged1 exposure.

Publication Title

RNA sequencing data of Notch ligand treated human dental pulp cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE15723
Gene profile in H1299 cells treated with PTD-DRBD GAPDH siRNA or treated with Lipofection GAPDH siRNA
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

Whole genome microarrays were probed with total mRNA from PTD-DRBD GAPDH siRNA treated H1299 cells at 12 h and 24 h. Using a 1.6x fold increase/decrease filter of cellular mRNAs, we detected a dramatic reduction in the target GAPDH mRNA along with a limited number of both up and down regulated genes. The up regulated genes were reduced in numbers and to nearly background 1.6x levels at 24 h, while the down regulated genes increased slightly in numbers and maintained a similar magnitude at 24 h. In contrast, lipofection treated cells showed both a dramatic increase in both the total number of genes altered and the magnitude of the increase. In addition, the numbers of genes affected increased between 12 h and 24 h, suggesting that lipofection of siRNAs into cells results in a substantial alteration to the transcriptome and may thereby confound interpretation of experimental outcomes. Moreover, the GAPDH specific knockdown was significantly smaller than PTD-DRBD mediated knockdown.

Publication Title

Efficient siRNA delivery into primary cells by a peptide transduction domain-dsRNA binding domain fusion protein.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE16265
SNEP: Simultaneous detection of nucleotide and expression polymorphisms using Affymetrix GeneChip
  • organism-icon Oryza sativa indica group
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Nucleotide polymorphisms can potentially influence the hybridization of mRNA to 25-mer oligonucleotides. Because Affymetrix Rice Genome Array was designated mainly for Nipponbare genome of Oryza sativa, the expression level of other varieties could not be estimated correctly. We tried to apply new approaches to estimate expression level by discerning the probe-level differential hybridization.

Publication Title

SNEP: Simultaneous detection of nucleotide and expression polymorphisms using Affymetrix GeneChip.

Sample Metadata Fields

Specimen part

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accession-icon GSE49782
Gene expression profiles of CD4 T cells and CD45+ HLA-DR+ cells during experimental allergic rhinitis in humans.
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Six patients with seasonal allergic rhinitis were challenged daily for 8 days with birch pollen extract. A mucosal biopsy was obtained from one nostril at basline (day 0) and from the other nostril after allergen challenge (day 9).

Publication Title

Rapid recruitment of CD14(+) monocytes in experimentally induced allergic rhinitis in human subjects.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP156330
Next generation sequencing facilities quantitative analysis of KMST6 cells expressing AUG-initiated c-Myc and CUG-initiated c-Myc.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To investigate the differences of transcriptional activities between AUG-initiated c-Myc and CUG-initiated c-Myc , we performed a transcriptomic analysis using high throoughput RNA sequencing (RNA-seq). Overall design: Total RNA extracted from KMST6 fibroblast cells stably expressing AUG-initiated c-Myc, CUG-initiated c-Myc, and empty vector (negative control) was subjected to RNA-seq analysis. The sequencing libraries generated from the RNA were analyzed by Illumina Hiseq 4000. The sequencing reads were trimmed for adaptor sequence, and low-complexity or low-quality reads were removed. Subsequently, the sequencing reads were aligned to the human reference GRCh38 genome using Gencode v27 annotations by STAR. Read counts per gene were quantified using the HTSeq Python package.

Publication Title

Novel oncogene 5MP1 reprograms c-Myc translation initiation to drive malignant phenotypes in colorectal cancer.

Sample Metadata Fields

Subject

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accession-icon SRP156328
Next generation sequencing facilities quantitative analysis of negative control HCT116 cells and 5MP1-overexpressed HCT116 cells.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

To investigate the downstream targets of eIF5 mimic protein 1 (5MP1), also known as Basic Leucine Zipper and W2 domains 2 (BZW2; Ensembl:ENSG00000136261), we performed a transcriptomic analysis using high throoughput RNA sequencing (RNA-seq). Overall design: Total RNA extracted from HCT116 cells stably expressing 5MP1 and empty vector-transfected negative control HCT116 cells was subjected to RNA-seq analysis. The sequencing libraries generated from the RNA were analyzed by Illumina Hiseq 4000. The sequencing reads were trimmed for adaptor sequence, and low-complexity or low-quality reads were removed. Subsequently, the sequencing reads were aligned to the human reference GRCh38 genome using Gencode v27 annotations by STAR. Read counts per gene were quantified using the HTSeq Python package.

Publication Title

Novel oncogene 5MP1 reprograms c-Myc translation initiation to drive malignant phenotypes in colorectal cancer.

Sample Metadata Fields

Subject

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accession-icon SRP174478
Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis. Overall design: Total RNA was extracted from the nontumor and tumor tissue of an Alb-Cre/Fbxl5F/F male mouse (nontumor, n = 5; tumor, n = 5) or two littermate control Fbxl5F/F mice (nontumor, n = 6; tumor, n = 6) at 45 weeks of age.

Publication Title

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE102863
Comparison of gene expression between Hep3B tumors treated with sorafenib plus mouse-IFN treatment and those treated with sorafenib alone
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In our experiments with a xenograft model, mouse-IFN (mIFN) treatment was suggested to exaggerate the antitumor effects of sorafenib on hepatocellular carcinoma in vivo.

Publication Title

The in vivo antitumor effects of type I-interferon against hepatocellular carcinoma: the suppression of tumor cell growth and angiogenesis.

Sample Metadata Fields

No sample metadata fields

View Samples

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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