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accession-icon GSE47504
Gene expresssion changes in pancreatic islets of 11 weeks old IKK2-CApdx-1 mice compared to control and Pdx-1+/- mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Canonical IKK/NF-B signaling is a master regulator of inflammation and innate immunity and has been implicated in the pathogenesis of T1D. To investigate the impact of NF-B activation on -cell homeostasis and diabetes development, we generated a transgenic gain-of-function mouse model allowing conditional NF-B activation via expression of IKK2-CA (constitutively active IKK2 allele) in -cells using the tetracycline-regulated gene expression system. Pdx-1-tTA (knockin model generating Pdx-1 haploinsufficiency) driver mice were used for -cell specific transgene expression. Double transgenic IKK2-CA-pdx-1 mice develop a full-blown immune-mediated diabetes.To identify gene expression changes underlying this diabetes development pancreatic islets of diabetic IKK2-CA-Pdx-1, PDX-1 +/- and control mice were prepared and isolated total RNA was used for microarray analysis.

Publication Title

Long-term IKK2/NF-κB signaling in pancreatic β-cells induces immune-mediated diabetes.

Sample Metadata Fields

Specimen part

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accession-icon GSE12400
Analysis of MYC in murine lymphoma cell lines
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MYC stimulates EZH2 expression by repression of its negative regulator miR-26a.

Sample Metadata Fields

Specimen part

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accession-icon GSE12278
MYC stimulates EZH2 expression by repression of its negative regulator miR-26a
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The MYC oncogene, which is commonly mutated/amplified in tumors, represents an important regulator of cell growth owing to its ability to induce both proliferation and apoptosis. Recent evidence links MYC to altered miRNA expression, thereby suggesting that MYC-regulated miRNAs might contribute to tumorigenesis. To further analyze the impact of MYC-regulated miRNAs we investigated a murine lymphoma model harboring the MYC transgene in a Tet-off system in order to control its expression. Microarray-based miRNA expression profiling revealed both known and novel MYC targets. Among the miRNAs repressed by MYC we identified the potential tumor suppressor miR-26a, which possessed the ability to attenuate proliferation in MYC-dependent cells. Interestingly, miR-26a was also found to be deregulated in primary human Burkitt lymphoma samples, thereby likely being of clinical relevance. While today only few miRNA targets have been identified in human disease, we could show that ectopic expression of miR-26a influenced cell cycle progression by targeting the bona fide oncogene EZH2, a Polycomb protein and global regulator of gene expression yet unknown to be regulated by miRNAs. Thus, in addition to directly targeting protein-coding genes, MYC modulates genes important to oncogenesis via deregulation of miRNAs, thereby vitally contributing to MYC-induced lymphomagenesis.

Publication Title

MYC stimulates EZH2 expression by repression of its negative regulator miR-26a.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE53124
Migration and invasion of 5 glioblastoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Glioblastoma cells are characterized by a highly invasive behavior whose mechanisms are not yet understood. Using the wound healing and Boyden chamber assays we compared in the present study the migration and invasion abilities of 5 glioblastoma cell lines (DK-MG, GaMG, U87-MG, U373-MG, SNB19) differing in p53 and PTEN status. We also analyzed by Western blotting the expression of PTEN, p53, mTOR and several other marker proteins involved in cell adhesion, migration and invasion. Among 5 cell lines, GaMG cells exhibited the fastest rate of wound closure, whereas U87-MG cells showed the most rapid chemotactic migration in the Boyden chamber assay. In DK-MG and GaMG cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG, U373-MG and SNB19 cells preferentially expressed F-actin in filopodia and lamellipodia. Moreover, the two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) were found to exhibit the fastest invasion rates through the Matrigel matrix.

Publication Title

Actin cytoskeleton organization, cell surface modification and invasion rate of 5 glioblastoma cell lines differing in PTEN and p53 status.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP185912
Inferring population dynamics from single-cell RNA-sequencing time-series data
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconNextSeq 500

Description

This dataset consists of single-cell RNA-seq (Drop-seq) data from thymi of day 14.5 mouse embryos. The sample includes the whole thymus, including mesenchyme, endothelium, epithelium, thymocytes, and other lymphocytes. The mouse is a Rag2-/- knockout. Overall design: 1 sample

Publication Title

Inferring population dynamics from single-cell RNA-sequencing time series data.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE38961
Gene expression of LDS-OECs
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The Loeys-Dietz syndrome (LDS) is an inherited connective tissue disorder caused by mutations in the transforming growth factor (TGF-) receptors TGFBR1 or TGFBR2. Most patients with LDS develop severe aortic aneurysms resulting in early need of surgical intervention. We investigated circulating outgrowth endothelial cells (OEC) from the peripheral blood of LDS to gain further insight into the pathophysiology of the disorder. We performed gene expression profiling using microarray analysis followed by quantitative PCR for verification of gene expression. OECs isolated from age- and sex-matched healthy donors served as reference control.

Publication Title

Overexpression of Gremlin-1 in patients with Loeys-Dietz syndrome: implications on pathophysiology and early disease detection.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE18632
Knockdown of transactive response DNA-binding protein TDP-43 downregulates histone deacetylase 6
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

TDP-43 is an RNA/DNA-binding protein implicated in transcriptional repression and mRNA processing. Inclusions of TDP-43 are hallmarks of frontotemporal dementias and amyotrophic lateral sclerosis. Besides aggregation of TDP-43, loss of nuclear localization is observed in disease. To identify relevant targets of TDP-43, we performed an expression profiling study. Thereby, histone deacetylase 6 (HDAC6) downregulation was discovered upon TDP-43 silencing on mRNA and protein level in human embryonic kidney HEK293E and neuronal SH-SY5Y cells. This was accompanied by accumulation of the major HDAC6 substrate, acetyl-tubulin. Expression of wild-type but neither RNA-binding- nor nuclear-localization-deficient TDP-43 restored HDAC6 expression. Moreover, TDP-43 bound specifically to HDAC6 mRNA arguing for a direct functional interaction. Importantly, in vivo validation in TDP-43 knockout Drosophila melanogaster also showed HDAC6 mRNA decrease. HDAC6 is necessary for protein aggregate formation and degradation. Indeed, downregulation of HDAC6 reduced aggregate formation and increased cytotoxicity of expanded poly-glutamine ataxin-3 in TDP-43 silenced cells. This was completely restored by co-transfection with HDAC6. In conclusion, loss of functional TDP-43 causes HDAC6 downregulation and might thereby contribute to pathogenesis.

Publication Title

Knockdown of transactive response DNA-binding protein (TDP-43) downregulates histone deacetylase 6.

Sample Metadata Fields

Cell line

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accession-icon SRP009043
Genome-wide Analysis of Nascent Transcription in Saccharomyces cerevisiae
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We combined the nuclear run-on (NRO) assay which labels and captures nascent transcripts with high throughput DNA sequencing to examine transcriptional activity in Saccharomyces cerevisiae. Overall design: Examination of nascent transcripts and steady-state transcripts in exponentially growing and heat-shock treated yeast.

Publication Title

Genome-Wide Analysis of Nascent Transcription in Saccharomyces cerevisiae.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE69862
Gene profiling of v-Src transformed primary chicken embryo fibroblasts (CEFs) under the condition of AP-1 repression
  • organism-icon Gallus gallus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

To investigate the role of AP-1 in Src-mediated transformation, we undertook a gene profiling study to characterize the transcriptomes of v-Src-transformed CEF expressing either the c-Jun dominant-negative mutant TAM67 or JunD shRNA.

Publication Title

JunD/AP-1 Antagonizes the Induction of DAPK1 To Promote the Survival of v-Src-Transformed Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE32614
Effects of Aging and Anatomic Location on Gene Expression in Human Retina
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective: To determine the effects of age and topographic location on gene expression in human neural retina.

Publication Title

Effects of aging and anatomic location on gene expression in human retina.

Sample Metadata Fields

Sex, Age

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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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Developed by the Childhood Cancer Data Lab

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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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