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accession-icon SRP073253
Transcriptomics of Kidney Cancer Samples
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptomics of Kidney Cancer Samples.

Publication Title

Targeting renal cell carcinoma with a HIF-2 antagonist.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon SRP170415
Cistromic re-programming by truncating GATA3 mutations promotes mesenchymal transformation in vitro, but not mammary tumour formation in mice [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Heterozygous mutations in the transcription factor GATA3 are identified in 10-15% of all breast cancer cases. Most of these are protein-truncating mutations, concentrated within or downstream of the second GATA-type zinc-finger domain. Here, we investigated the functional consequences of expression of two truncated GATA3 mutants, in vitro in breast cancer cell lines and in vivo in the mouse mammary gland. We found that the truncated GATA3 mutants display altered DNA binding activity caused by preferred tethering through FOXA1. In addition, expression of the truncated GATA3 mutants reduces E-cadherin expression and promotes anchorage-independent growth in vitro. However, we could not identify any effects of truncated GATA3 expression on mammary gland development or mammary tumor formation in mice. Together, our results demonstrate that both truncated GATA3 mutants promote cistromic re-programming of GATA3 in vitro, but these mutants are not sufficient to induce tumor formation in mice. Overall design: RNAseq data of T47D cells expressing HA-tagged wild-type GATA3 (HA_GATA3_wt) or one of two truncated variants (HA_GATA3_TR1 and HA_GATA3_TR2).

Publication Title

GATA3 Truncating Mutations Promote Cistromic Re-Programming In Vitro, but Not Mammary Tumor Formation in Mice.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE1009
Diabetic nephropathy
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy

Publication Title

Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12211
Gene expression of CML CD34+ cells during Imatinib therapy
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Imatinib has become the current standard therapy for patients with chronic myelogenous leukaemia (CML). For a better understanding of the Imatinib-related molecular effects in vivo, we assessed gene expression profiles of Philadelphia Chromosome positive (Ph+) CD34+ cells from peripheral blood of 6 patients with de novo CML in chronic phase. After 7 days of treatment with Imatinib the Ph+ CD34+ cells were reassessed to look for changes in the transcriptome. The expression level of 303 genes was significantly different comparing the transcriptome of the Ph+ CD34+ cells before and after 7 days of Imatinib therapy (183 down-regulated, 120 up-regulated, lower bound 1.2-fold). For a substantial number of genes governing cell cycle and DNA replication, the level of expression significantly decreased (CDC2, RRM2, PCNA, MCM4). On the other hand, therapy with Imatinib was associated with an increase of genes related to adhesive interactions, such as L-selectin or CD44. A group of 8 genes with differential expression levels were confirmed using a gene specific quantitative real-time PCR. Thus, during the first week of treatment, Imatinib is preferentially counteracting the bcr-abl induced effects related to a disturbed cell cycle and defective adhesion of leukemic Ph+ CD34+ cells.

Publication Title

Early in vivo changes of the transcriptome in Philadelphia chromosome-positive CD34+ cells from patients with chronic myelogenous leukaemia following imatinib therapy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13810
Microarray analysis of the development of proteinuria in the Dahl salt-sensitive rat
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

To get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain.

Publication Title

Increased dynamin expression precedes proteinuria in glomerular disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE57028
Transcriptomics of vitamin D treatment effects in Mycobacterium tuberculosis-infected THP-1 cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Previous reports have shown low vitamin D serum levels and polymorphisms in the vitamin D receptor (VDR) to be associated with increased risk for TB. Given that 1,25-dihydroxyvitamin D3 has a role in lipid metabolism control, we tested whether the link between 1,25-dihydroxyvitamin D3 and tuberculosis involves macrophage lipid metabolism. Since formation of lipid droplets (LD) is a hallmark of lipid dysregulation in M. tuberculosis-infected macrophages, we measured LD content as a readout of altered lipid metabolism in infected THP-1 cells. Induction of LD, which peaked by 24 hours post-infection was prevented by addition of 1,25-dihydroxyvitamin D3 at the time of infection. To investigate the mechanism of 1,25-dihydroxyvitamin D3 modulation of LD formation, we analyzed the transcriptome of M. tuberculosis-infected THP-1 cells with and without 1,25-dihydroxyvitamin D3 treatment.

Publication Title

Cutting edge: Vitamin D regulates lipid metabolism in Mycobacterium tuberculosis infection.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE22656
Expression data from CD71+ cells from the bone marrow of WT, CD70TG, IFNg-/- and CD70TG*IFNg-/- mice.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CD70TG mice are a model for sterile chronic immune activation and develop Anemia of Inflammation, which is dependent on the production of Ifng by effector CD4 and CD8 T cells.

Publication Title

Chronic IFN-γ production in mice induces anemia by reducing erythrocyte life span and inhibiting erythropoiesis through an IRF-1/PU.1 axis.

Sample Metadata Fields

Specimen part

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accession-icon GSE99358
The role of FAM46C in myeloma cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HiSeq 2000

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Loss of <i>FAM46C</i> Promotes Cell Survival in Myeloma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE99357
The role of FAM46C in myeloma cells [array]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

FAM46C is one of the most recurrently mutated genes in multiple myeloma (MM), however its role in disease pathogenesis is not determined. Here we demonstrate that wild type (WT) FAM46C overexpression induces substantial cytotoxicity in MM cells. In contrast, FAM46C mutations found in MM patients abrogate this cytotoxicity indicating a MM survival advantage conferred by the FAM46C mutant phenotype. WT FAM46C overexpression downregulated IRF4, CEBPB, MYC and upregulated immunoglobulin (Ig) light chain and HSPA5/BIP. Furthermore, pathway analysis suggests that enforced FAM46C expression activates the unfolded protein response (UPR) pathway and induces mitochondrial dysfunction. In contrast, endogenous CRISPR FAM46C depletion enhanced MM cell growth and notably decreasing Ig light chain and BIP expression, activating of ERK and anti-apoptotic signaling and conferring relative resistance to dexamethasone and lenalidomide treatment. The genes altered in FAM46C depleted cells are enriched for signaling pathways regulating estrogen, glucocorticoid, B cell receptor signaling and ATM signaling. Together these results implicate FAM46C in myeloma cell growth and survival. FAM46C mutation contributes to myeloma pathogenesis and disease progression by perturbation in plasma cell differentiation and endoplasmic reticulum homeostasis.

Publication Title

Loss of <i>FAM46C</i> Promotes Cell Survival in Myeloma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP200560
RNAseq of haemogenic and aortic endothelium in zebrafish embryos 28-20 hours post fertilization
  • organism-icon Danio rerio
  • sample-icon 42 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The goal of this study is to perform RNAseq in different sub-types of the zebrafish embryonic dorsal aorta (DA) at 28-30 hpf using TgBAC(runx1P2:Citrine);Tg(kdrl:mCherry) double-transgenic zebrafish embryos. A min. of 3000 cells per population were collected via FACS. RNA was isolated with the RNeasy Plus Micro Kit (QIAGEN, Cat No. 74034). High quality RNA (RIN > 8.0) was sent for RNAseq to the Wellcome Trust Centre for Human Genetics (WTCHG). 2.2 ng of total RNA was used to generate SMARTer libraries for low-input RNA. Sequencing was performed on an Illumina HiSeq4000 machine with a 75 bp paired end protocol. Sequenced reads were checked for base qualities, trimmed where 20% of the bases were below quality score 20, and filtered to exclude adapters using Trimmomatic (Version 0.32). Sequences were aligned to the Zebrafish Genome Zv10 with STAR with default parameters. Aligned read features were counted using Subread tool: featureCounts method (version 1.4.5-p1). To determine number of mapped reads we used the trimmed data. The alignment has been performed using STAR with default parameters. The number of mapped reads (QC-passed reads count) has been obtain using Samtools mapping statistics (flagstat tool). Overall design: Analysis of 5 different cell types; DN (double negative), SP-kdrl (single positive), DP-R1lo (double positive runx1 low expression), DP-R1med (runx1 medium expressionand) and DP-R1hi (runx1 high expression) in non-injected (Wt) TgBAC(runx1P2:Citrine);Tg(kdrl:mCherry) double-transgenic zebrafish embryos. Analysis was also done of the DN and DP-R1hi populations in runx1-morpholino (MO) injected embryos.

Publication Title

Blood stem cell-forming haemogenic endothelium in zebrafish derives from arterial endothelium.

Sample Metadata Fields

Specimen part, 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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