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accession-icon GSE71194
Muscle expression of SOD1G93A modulates microRNA and mRNA expression pattern associated with the myelination process in the spinal cord of transgenic mice.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE43053
The multikinase inhibitor Sorafenib targets mitochondria and synergizes with glycolysis blockade for cancer cell killing.
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Objective: identify novel and relevant aspects of Sorafenib action on liver cancer cells. We found that in rat hepatocholangiocarcinoma (LCSC-2) cells, exposure to the MEK/multikinase inhibitor sorafenib did not inhibit ERK phosphorylation nor induced appreciable cell death in the low micromolar range; instead, the drug elicited a raise of intracellular reactive oxygen species (ROS) accompanied by a severe decrease of oxygen consumption and intracellular ATP levels, all changes consistent with mitochondrial damage. Moreover, Sorafenib induced depolarization of isolated rat liver mitochondria, indicating a possible direct effect on the organelle. Microarray analysis of gene expression in sorafenib-trated cells revealed a metabolic reprogramming toward aerobic glycolysis, that likely accounts for resitance to drug toxicity in this cell line. Importantly, cytotoxicity was strongly potentiated by glucose withdrawal from the culture medium or by the glycolytic inhibitor 2-deoxy-glucose, a finding also confirmed in the highly malignant melanoma cell line B16F10. Mechanistic studies revealed that ROS are pivotal to cell killing by the Sorafenib + 2DG combination, and that a low content of intracellular oxidants is associated with resistance to the drug; instead, Thr172phosphorylation/activation of the AMP-activated protein kinase (AMPK), induced by Sorafenib, may exert protective effects, since cytotoxicity was enhanced by an AMPK specific inhibitor and prevented by the AMPK activator Metformin. Overall, this study identifies novel and relevant aspects of Sorafenib action on liver cancer cells, including mitochondrial damage, induction of ROS and a metabolic cell reprogramming towards glucose addiction, potentially exploitable in therapy.

Publication Title

The multikinase inhibitor Sorafenib enhances glycolysis and synergizes with glycolysis blockade for cancer cell killing.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE6011
Expression data from quadriceps muscle of young DMD patients and age matched controls
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Albeit increased serum CK level and abnormal muscle histology are always present, boys with DMD are phenotipically indistinguishable from the normal ones at birth and, in their first years of life, acquire early motor milestones at normal times. A clear defect in muscle function becomes generally apparent by the end of the second year. As the disease is typically diagnosed between the ages of 3 and 7, the first two years are often considered and referred to as clinically presymptomatic.

Publication Title

Gene expression profiling in the early phases of DMD: a constant molecular signature characterizes DMD muscle from early postnatal life throughout disease progression.

Sample Metadata Fields

Sex, Age

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accession-icon SRP068229
miRNAs affected by antagomiR-17 treatment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

To understand the the effect of antagomir-17 treatment on human endothelial cells derived from human umbilical cord blood (UCB) CD34+ hematopoietic stem cells, we have employed mRNA sequencing. The antagomiR-17 used in this study was purchased from Dharmacon and cell transfection was performed using Lipofectamine RNAiMAx from Life Technologies. Scramble antagomiR from Ambion was used as control. Cells were transfected with antagomiR-17 or scrambled antagomiR for 48 hours. After 48 h, the cells were collected, RNA was isolated and RNA samples were shipped to Exiqon Services, Denmark for mRNA sequencing. All sequencing experiments (RNA integrity measurements, library preparation and next generation sequencing) were conducted at Exiqon Services, Denmark. Overall design: CD34+ endothelial cells differentiated from umbilical cord blood hematopoietic stem cells (CD34+) were treated with 50 nM antagomiR-17 (Dharmacon) or scrambled antagomiR (Ambion) using Lipofectamine RNAiMAx (Life Technologies) for 48 h. Three replicates were used for each condition (i.e. antagomiR-17 and scramble antagomiR conditions).

Publication Title

Synthetic microparticles conjugated with VEGF<sub>165</sub> improve the survival of endothelial progenitor cells via microRNA-17 inhibition.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP135885
Effect of mutant TRP53 proteins on nutlin-3a treated mouse lymphoma cell lines (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 131 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Mutations in TRP53, prevalent in human cancers, reportedly drive tumorigenesis through dominant-negative-effects (DNE) over wt TRP53 and neomorphic gain-of-function (GOF) effects. We show that five TRP53 mutants do not accelerate lymphomagenesis on a TRP53-deficient background but strongly synergize with c-MYC over-expression. RNA-seq analysis revealed that mutant TRP53 does not globally repress wt TRP53 function but exerts a DNE with disproportionate impact on subsets of wt TRP53 target genes, particularly those involved in DNA repair, proliferation and metabolism. This reveals that the mutant TRP53 DNE drives tumorigenesis by modulating wt TRP53 function in a manner that is advantageous for neoplastic transformation. Overall design: Each of 5 mutant human TRP53 proteins, and a negative control, was expressed in 3 mouse lymphoma cell lines, both before and after activation of WT TRP53 with nutlin-3a.

Publication Title

Mutant TRP53 exerts a target gene-selective dominant-negative effect to drive tumor development.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE79386
Comparative tissue gene expression profiling and alternative splicing by exon-sensitive microarrays in non-syndromic craniosynostosis
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Craniosynostosis (CS) is the congenital premature fusion of one or more cranial sutures and represents the more prevalent craniofacial malformation in humans, with an overall incidence of 1 out of 2000-3000 live births. Non-syndromic craniosynostoses (NSC) are believed to be multifactorial disorders, with a strong genetic component, due to possible genegene or geneenvironment interactions that remain to be clearly identified. In this study we delved into the molecular signaling acting in calvarial tissue and cells from patients affected by nonsynodromic midline craniosynostosis, using a comparative analysis between fused and unfused sutures of each affected individuals. Using comparative microarray tissue gene expression profiling we have identified a subset of genes involved in the structure and function of the primary cilium, including the Bardet-Biedl syndrome 9 (BBS9) gene, which was recently associated to sagittal synostosis in a GWAS study. We therefore characterized BBS9 expression and cilium-related signaling in cells isolated from patients calvarial bone.

Publication Title

BBS9 gene in nonsyndromic craniosynostosis: Role of the primary cilium in the aberrant ossification of the suture osteogenic niche.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon SRP019249
CLIP-seq of S. cerevisiae Drn1-TAP and Dbr1-TAP
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

Data for replicate Drn1-TAP and Dbr1-TAP CLIP-seq experiments to identify RNA-protein interactions Overall design: Drn1-TAP and Dbr1-TAP CLIP-seq

Publication Title

A homolog of lariat-debranching enzyme modulates turnover of branched RNA.

Sample Metadata Fields

Disease, Subject

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accession-icon SRP058647
Mastermind-like 3 controls proliferation and differentiation in neuroblastoma (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Neuroblastoma cell lines can differentiate upon retinoic acid (RA) treatment, a finding that provided the basis for the clinical use of RA to treat neuroblastoma. However, resistance to RA is often observed, which limits its clinical utility. Using a gain-of-function genetic screen we identify the transcriptional coactivator Mastermind-like 3 (MAML3) as a gene whose ectopic expression confers resistance to RA. We find that MAML3 expression leads to loss of activation of a subset of RA target genes, which hampers RA-induced differentiation. The regulatory DNA elements of this subset of RA target genes show overlap in binding of MAML3 and the retinoic acid receptor, suggesting a role for MAML3 in the regulation of these genes. In addition, MAML3 has RA independent functions, including the activation of IGF1R and downstream AKT signaling via upregulation of IGF2, resulting in increased proliferation. Our results indicate an important role for MAML3 in differentiation and proliferation of neuroblastomas. Overall design: RNA-seq of SK-N-SH control and MAML3 overexpressing (SD3.23) cells, either untreated (UT) or treated with 1 µM RA (RA).

Publication Title

Mastermind-Like 3 Controls Proliferation and Differentiation in Neuroblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP073181
Single cell sequencing of Dgcr8 knockout embryonic stem cells plus/minus miR-294 or let-7
  • organism-icon Mus musculus
  • sample-icon 232 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed Fluidigm C1 single cell sequencing analysis of wild-type and microRNA deficient (Dgcr8 knockout) mouse embryonic stem cells mock treated or transfected with either miR-294 or let-7. Overall design: Wild-type and Dgcr8 knockout cells grown in naïve culture conditions were mock transfected or transfected with miRNA mimics for let-7b or miR-294, single cells were captured on Fluidigm C1 24 hours post-transfection and then prepared for sequencing on Illumina HiSeq1000 following manufacturer''s protocol.

Publication Title

The impact of microRNAs on transcriptional heterogeneity and gene co-expression across single embryonic stem cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE30531
Expression data of A375 melanoma cells after DMSO or MLN4924 treatment from 1 hour to 24 hour
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarrays were used to determine the change in gene expression of genes involved in the CDT1/NAE pathway

Publication Title

Quantitative proteomic analysis of cellular protein modulation upon inhibition of the NEDD8-activating enzyme by MLN4924.

Sample Metadata Fields

Cell line, Treatment, Time

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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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