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accession-icon GSE40883
Gene expression before or 3 hours after t-RA treatment in HeLa cells expressing an shRNA control or shRNA against PARG
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The goal of this experiment was to compare gene expression after t-RA treatment in cells with or without the presence of the PolyADP ribose Glycohydrolase protein (PARG)

Publication Title

Poly (ADP-ribose) glycohydrolase regulates retinoic acid receptor-mediated gene expression.

Sample Metadata Fields

Cell line

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accession-icon SRP059266
TALENs-mediated gene disruption of FLT3 in leukemia cells: Using genome-editing approach for exploring the molecular basis of gene abnormality
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Novel analytic tools are needed to elucidate the molecular basis of leukemia-relevant gene mutations in the post-genome era. We generated isogenic leukemia cell clones in which the FLT3 gene was disrupted in a single allele using TALENs. Isogenic clones with mono-allelic disrupted FLT3 were compared to an isogenic wild-type control clone and parental leukemia cells for transcriptional expression, downstream FLT3 signaling and proliferation capacity. The global gene expression profiles of mutant K562 clones and corresponding wild-type controls were compared using RNA-seq. The transcriptional levels and the ligand-dependent autophosphorylation of FLT3 were decreased in the mutant clones. TALENs-mediated FLT3 haplo-insufficiency impaired cell proliferation and colony formation in vitro. These inhibitory effects were maintained in vivo, improving the survival of NOD/SCID mice transplanted with mutant K562 clones. Cluster analysis revealed that the gene expression pattern of isogenic clones was determined by the FLT3 mutant status rather than the deviation among individual isogenic clones. Differentially expressed genes between the mutant and wild-type clones revealed an activation of nonsense-mediated decay pathway in mutant K562 clones as well as an inhibited FLT3 signaling. Our data support that this genome-editing approach is a robust and generally applicable platform to explore the molecular bases of gene mutations. Overall design: Global gene expression profiles of three isogenic K562 mutant clones (clones k20, k112, k324) and three randomly selected wild-type clones (clones kw1, kw2, kw3) were generated by RNA-seq, using Illumina Hiseq 2000.

Publication Title

TALENs-mediated gene disruption of FLT3 in leukemia cells: Using genome-editing approach for exploring the molecular basis of gene abnormality.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41638
Microarray analysis of WT and Drd2-/- striatal tissue from C57BL/6 mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Drd2 regulates striatal gene networks.

Publication Title

Suppression of neuroinflammation by astrocytic dopamine D2 receptors via αB-crystallin.

Sample Metadata Fields

Specimen part

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accession-icon SRP105328
Temporal Transcriptome Analysis of Pancreatic ß-Cells in Response to Lipotoxicity and Glucolipotoxicity.
  • organism-icon Rattus norvegicus
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The pancreatic beta cell function failure is the core event of type 2 diabetes mellitus. High levels of free fatty acid and glucose are two main factor that induced pancreatic beta cell function failure. Long term exposure to palmitate can induced pancreatic beta cell apoptoss and impaired insulin secretion in vivo and in vitro, called lipotoxicity. The lipotoxicity often coupled with high glucose, their combination form called glucolipotoxcity. We carried out temporal transcriptome and proteome studies investigating the evolution of molecular events in Ins1 cells stimulated by palmitate for different times. And through compared the transcriptome and proteome between lipotoxicity and glucolipotoxicity explain the mechanism of glucolipotoxicity more harmfull to beta cell. Overall design: we performed a time-course large-scale transcriptome of INS1 cells induced by 0.5 mM palmitate and 0.5 mM palmitate with 27.8 mM glucose at four time points (8, 16, 24 and 48 h) using MAPS method

Publication Title

Temporal Proteomic Analysis of Pancreatic β-Cells in Response to Lipotoxicity and Glucolipotoxicity.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE71459
Different expression patterns in leukemia cells caused by decreased expression of TNF-
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To design an effective antibody therapy to improve clinical outcomes in leukemia, the identification of novel cell surface antigens is needed. Herein, we demonstrate a role for transmembrane tumor necrosis factor-in leukemia. To characterize tmTNF- expression in acute leukemia, normal hematopoietic cells, and non-hematopoietic tissues, we used a monoclonal antibody, termed C1, which specifically recognizes the tmTNF- domain. We found that tmTNF- was preferentially expressed by acute leukemia and leukemia stem cells. More abundant expression correlated with poor risk stratification, extramedullary infiltration, and adverse clinical parameters. Moreover, knockdown of tmTNF-+ expression rendered leukemia cells more sensitive to chemotherapy in vitro and delay regeneration of leukemia in NODSCID mice. Targeting tmTNF- by C1 resulted in leukemia cell killing via antibody-dependent cell-mediated and complement -dependent cytotoxicity in vitro, and inhibited leukemia cell growth in vivo while simultaneously sparing normal hematopoietic cells. Notably, C1 administration impaired the regeneration of leukemia in secondary serial transplantationin to NOD-SCID mice.

Publication Title

Transmembrane TNF-α preferentially expressed by leukemia stem cells and blasts is a potent target for antibody therapy.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE155206
Expression data from ectopic expression of ACAT1 in Nasopharyngeal carcinoma (NPC) cell lines
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Compare with normal nasopharyngeal epithelial cells, we found ACAT1 was decreased in NPC cells, we found that ACAT1 inhibited proliferation, colony formation, migration and invasion in NPC cells. We used microarrays to identify differential genes regulated by ACAT1 in NPC cell lines.

Publication Title

Epigenetic Inactivation of Acetyl-CoA Acetyltransferase 1 Promotes the Proliferation and Metastasis in Nasopharyngeal Carcinoma by Blocking Ketogenesis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP075578
Regulation of DNA methylation landscape in human somatic cell reprogramming by miR-29 family (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Reprogramming to pluripotency after overexpression of OCT4, SOX2, KLF4 and MYC is accompanied by global genomic and epigenomic changes. Histone modification and DNA methylation states in iPSCs have been shown to be highly similar with embryonic stem cells (ESCs). However, epigenetic differences still exist between iPSCs and ESCs. In particular, aberrant DNA methylation states found in iPSCs are a major concern for using iPSCs in a clinical setting. Thus, it is critical to find factors that regulate DNA methylation states in reprogramming. Here, we found that the miR-29 family is an important epigenetic regulator during human somatic cell reprogramming. Our global DNA methylation and hydroxymethylation analysis shows that DNA demethylation is a major event mediated by miR-29a depletion during early reprogramming, and that iPSCs derived from miR-29a depletion are epigenetically closer to ESCs. Our findings uncover an important miRNA-based approach to generate clinically robust iPSCs. Overall design: Bisulphite converted gDNAs of D551 fibroblasts transduced for 3 days with overexpression of DNMTs, TETs, TDG and OSKM or miR29a/b/c and control sponge were hybridized into Illumina Infinium HumanMethylation 450K Beadchip.

Publication Title

Regulation of the DNA Methylation Landscape in Human Somatic Cell Reprogramming by the miR-29 Family.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE105763
MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-cell Acute Lymphoblastic Leukemia
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Little is known about the roles of methyl-CpG-binding domain protein 2 (MBD2), a reader of DNA methylation, in T-cell acute lymphoblastic leukemia (T-ALL). Here, we investigated the role of MBD2 in T-ALL by using an Mbd2 knockout mouse model. We found that MBD2 ablation impeded the progression and maintenance of Notch1-driven T-ALL.Our data reveals essential roles for MBD2 in lymphopoiesis and T-ALL and support an intriguing potential of MBD2 as a therapeutic target for T-ALL.

Publication Title

MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-ALL.

Sample Metadata Fields

Specimen part

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accession-icon GSE25073
Expression data from rice seedlings of wild type and the CHR729 mutant
  • organism-icon Oryza sativa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

In order to study the function of CHR729 in rice, the T-DNA insertion mutant of CHR729 was obtained and analysed.

Publication Title

CHD3 protein recognizes and regulates methylated histone H3 lysines 4 and 27 over a subset of targets in the rice genome.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP010350
Effects of Cardiac Glycosides on RNA Expression in Prostate Cancer LNCaP-abl Cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Illumina HiSeq 2000

Description

Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown. Overall design: Observation of three cardioglycosides, Digoxin, Peruvoside and Strophanthidin, and AR knockdown regulated RNA expression in LNCaP-abl with RNA-Seq (each triplicates)

Publication Title

Versatile pathway-centric approach based on high-throughput sequencing to anticancer drug discovery.

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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