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accession-icon GSE86416
MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE86407
MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [microarray]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We address the molecular mechanisms through which MYC promotes loss of cell identity and acquisition of stem cell-like traits, favouring the onset of tumorigenesis, by performing gene expression profile analyses in a transition from WT IMEC, IMEC over-expressing MYC and mammospeheres formed from IMEC-MYC (named M2). We then investigated the global gene expression profile of the fraction of cells hyper-activating the WNT pathway in M2 spheres, compared to the ones with low activation

Publication Title

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP059948
Transcriptome-wide mapping of cut sites of the viral endoribonuclease SOX from Kaposi''s sarcoma-associated herpesvirus (KSHV)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Purpose: identify sites in endogenous mRNAs that are cut by KSHV SOX; Method: parallel analysis of RNA ends (PARE, following Zhai et al., 2014); Results: SOX cuts at discrete locations in mRNAs Overall design: human Xrn1 was knocked down in HEK293T cells by shRNAs or siRNAs to stabilize degradation fragments with free 5'' ends; GFP-SOX or GFP were transfected for ~24 hrs; total RNA samples were collected and subjected to PARE protocol (Zhai et al., 2014)

Publication Title

Transcriptome-Wide Cleavage Site Mapping on Cellular mRNAs Reveals Features Underlying Sequence-Specific Cleavage by the Viral Ribonuclease SOX.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP197582
Time-series reveals processes underlying colon inflammation and repair
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To elucidated through an unbiased manner which genes and pathways are differentially regulated during mouse colonic inflammation followed by a tissue regeneration phase. In particular, we took advantage of the widely used dextran sodium sulfate (DSS)-induced model of colitis. This model is one of the few characterized by a phase of damage followed by a phase of regeneration. Therefore, this model gave the possibility to identify also sets of genes essential in the regeneration phase, a key step towards the resolution of the inflammation. In short, mice were exposed to DSS in the drinking water for 7 days, then allowed to recover for the following 7 days. During this period, we collected colonic tissue samples every second day to then be analyzed by RNA sequencing (RNA-seq). Next, we performed a RNA-seq analysis from colonic samples throughout the experiment and computed differentially expressed genes (DEGs) taking the complete kinetics of expression into consideration for p-value estimation using EdgeR. Overall design: C57BL/6J female mice were treated with 2.5% DSS in order to induce colinic inflammation. 2-3 animals were sacrificed at different time points when the colonic tissue was collected.

Publication Title

Conserved transcriptomic profile between mouse and human colitis allows unsupervised patient stratification.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE118907
Esrrb extinction triggers dismantling of nave pluripotency and marks commitment to differentiation.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Esrrb extinction triggers dismantling of naïve pluripotency and marks commitment to differentiation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE118906
Esrrb extinction triggers dismantling of nave pluripotency and marks commitment to differentiation [Microarray]
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Self-renewal of embryonic stem cells (ESCs) cultured in serum-LIF is incomplete with some cells initiating differentiation. While this is reflected in heterogeneous expression of naive pluripotency transcription factors (TFs), the link between TF heterogeneity and differentiation is not fully understood. Here we purify ESCs with distinct TF expression levels from serum-LIF cultures to uncover early events during commitment from nave pluripotency. ESCs carrying fluorescent Nanog and Esrrb reporters show Esrrb downregulation only in NANOGlow cells. Independent Esrrb reporter lines demonstrate that ESRRBnegative ESCs cannot effectively self-renew. Upon ESRRB loss, pre-implantation pluripotency gene expression collapses. ChIP-Seq identifies different regulatory element classes that bind both OCT4 and NANOG in ESRRBhigh cells. Class I elements lose NANOG and OCT4 binding in ESRRBnegative ESCs and associate with genes expressed preferentially in nave ESCs. In contrast, class II elements retain OCT4 but not NANOG binding in ESRRBnegative cells and associate with more broadly expressed genes. Therefore, mechanistic differences in TF function act cumulatively to restrict potency during exit from nave pluripotency.

Publication Title

Esrrb extinction triggers dismantling of naïve pluripotency and marks commitment to differentiation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE3126
Comparison of HNF4 null mouse embryonic livers with control mouse embryonic livers
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To study the role of hepatic nuclear factor alpha (HNF4a in hepatogenesis, we used loxP-Cre technology to eliminate it from developing mouse livers.

Publication Title

Hepatocyte nuclear factor 4alpha orchestrates expression of cell adhesion proteins during the epithelial transformation of the developing liver.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE29962
Nutrient-dependent growth of NIH3T3 and NIH3T3 K-ras cell lines.
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiling of normal NIH3T3 and transformed NIH3T3 K-ras cell lines grown for 72 hours in optimal glucose availability (25 mM glucose) or low glucose availability (1 mM). Low glucose induces apoptosis in transformed cells as compared to normal ones.

Publication Title

Oncogenic K-Ras decouples glucose and glutamine metabolism to support cancer cell growth.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE2470
Gene expression profile of tungstate-induced beta cell mass increase in STZ rats
  • organism-icon Rattus norvegicus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Background and Aims: It is well demonstrated that in the beta cell population of the pancreas there is a dynamic turnover, which results from the net balance of several processes; beta cell replication, apoptosis and neogenesis. These processes have been studied in partial pancreatectomy and glucagon-like peptide 1 treated animals, where an increase in pancreas regeneration has been observed. Similarly, sodium tungstate, which decreases hyperglycemia in several animal models of diabetes, promotes a rise in the beta cell mass of nSTZ and STZ animals. However, the molecular mechanisms underlying this pancreas regeneration remain unknown. Therefore the objective of this study is to identify which genes are up or down regulated in the increase of the beta cell population of STZ rats treated with sodium tungstate.

Publication Title

Molecular mechanisms of tungstate-induced pancreatic plasticity: a transcriptomics approach.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP162136
Profiling of RNAs downregulated by influenza A virus PA-X ribonuclease
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this analysis was to investigate the targets of the influenza A host shutoff ribonuclease PA-X. We profiled the relative levels of cellular RNAs in cells infected with influenza A virus (A/PuertoRico/8/1934 H1N1) comparing wild-type and mutants that make reduced levels of PA-X and/or make a truncated and inactive PA-X. We also profiled relative RNA levels in cells overexpressing wild-type PA-X or a catalytically inactive mutant (D108A). Overall design: for extopic expression, PA-X (from the A/PuertoRico/8/1934 H1N1 (PR8) strain) was expressed in A549 cells using a doxycyline-inducible transgene for 18 hrs; for infection, A549 cells were infected with the wild-type PR8 strain or mutant strain that carried mutations that reduce PA-X production or activity for 15 hrs. rRNA deplete RNA was subjected to high-throughput sequencing

Publication Title

The Influenza A Virus Endoribonuclease PA-X Usurps Host mRNA Processing Machinery to Limit Host Gene Expression.

Sample Metadata Fields

Treatment, 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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