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accession-icon GSE77867
Combined blockade of MET and EGFR abolishes liver regeneration
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Receptor tyrosine kinases MET and EGFR are critically involved in initiation of liver regeneration. Other cytokines and signaling molecules also help in the early part of the process. Regeneration employs effective redundancy schemes to compensate for missing signals. Elimination of any single signaling pathway only delays but does not abolish the process. Our present study, however, shows that combined systemic elimination of MET and EGFR signaling abolishes liver regeneration, prevents restoration of liver mass and leads to liver decompensation. Our results demonstrate that liver function is dependent on synchronous availability of signaling from these two pathways. The study shows that MET and EGFR separately control many non-overlapping signaling endpoints, allowing for compensation when only one of the signals is blocked. The combined elimination of the signals however was not tolerated. The results provide critical new information on interactive MET and EGFR signaling and the contribution of their combined absence to regeneration arrest and liver decompensation.

Publication Title

Combined systemic elimination of MET and epidermal growth factor receptor signaling completely abolishes liver regeneration and leads to liver decompensation.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP057586
Unbiased evaluation of cell-free amniotic fluid transcriptome of term and preterm infants to detect fetal maturity
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Objective: Amniotic fluid (AF) is a proximal fluid to the fetus containing higher amounts of cell-free fetal RNA/DNA than maternal serum, thereby making it a promising source for novel biomarker discovery of fetal development and maturation. Our aim was to compare AF transcriptomic profiles at different time points in pregnancy to demonstrate unique genetic signatures that would serve as potential biomarkers indicative of fetal maturation. Methods: We isolated AF RNA from 16 women at different time points in pregnancy: 4 from 18-24 weeks, 6 from 34-36 weeks, and 6 from at 39-40 weeks. RNA-sequencing was performed on cell-free RNA. Gene expression and splicing analyses were performed in conjunction with cell-type and pathway inference.  Results: Sample-level analysis at different time points in pregnancy yielded a strong correlation with cell types found in the intrauterine environment and fetal respiratory, digestive and external barrier tissues of the fetus, using high-confidence cellular molecular markers. While some genes and splice variants were present throughout pregnancy, an abundant number of transcripts were uniquely expressed at different time points in pregnancy and associated with distinct fetal co-morbidities (respiratory distress and gavage feeding), indicating fetal immaturity. Conclusions: The AF transcriptome exhibits unique cell- and organ-selective expression patterns at different time points in pregnancy that can potentially identify fetal organ maturity and predict neonatal morbidity. Developing novel biomarkers indicative of the maturation of multiple organ systems can improve upon our current methods of fetal maturity testing which focus solely on the lung, and better inform obstetrical decisions regarding delivery timing. Overall design: RNA-Seq from cell-free was used to idenitfy mRNA transcripts indicative of overall fetal maturity.

Publication Title

Systems biology evaluation of cell-free amniotic fluid transcriptome of term and preterm infants to detect fetal maturity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49804
Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone

Publication Title

Caveolin-1 regulates genomic action of the glucocorticoid receptor in neural stem cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP074235
Opposing Effects of Cyclooxygenase-2 (COX-2) on Estrogen Receptor ß (ERß) Response to 5a-reductase Inhibition in Prostate Epithelial Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Current pharmacotherapies for symptomatic benign prostatic hyperplasia (BPH), an androgen receptor (AR) driven, inflammatory disorder affecting elderly men, include 5a-reductase (5AR) inhibitors (i.e. dutasteride and finasteride) to block the conversion of testosterone to the more potent AR ligand dihydrotestosterone (DHT). Since DHT is the precursor for estrogen receptor ß (ERß) ligands, 5AR inhibitors could potentially limit ERß activation, which maintains prostate tissue homeostasis. We have uncovered signaling pathways in BPH-derived prostate epithelial cells (BPH-1) that are impacted by 5AR inhibition. The induction of apoptosis and repression of the cell-adhesion protein E-cadherin by the 5AR inhibitor, dutasteride, requires both ERß and TGFß. Dutasteride also induces cyclooxygenase type 2 (COX-2), which functions in a negative-feedback loop in TGFß and ERß signaling pathways as evidenced by the potentiation of apoptosis induced by dutasteride or finasteride upon pharmacological inhibition or shRNA-mediated ablation of COX-2. Concurrently, COX-2 positively impacts ERß action through its effect on the expression of a number of steroidogenic enzymes in the ERß-ligand metabolic pathway. Therefore, effective combination pharmacotherapies, which have included non-steroidal anti-inflammatory drugs, must take into account biochemical pathways affected by 5AR inhibition and opposing effects of COX-2 on the tissue protective action of ERß. Overall design: Next-generation sequencing (n=3) of shRNA mediated knockdown of COX-2 or scrambled control in BPH-1 prostate epithelial cell line

Publication Title

Opposing Effects of Cyclooxygenase-2 (COX-2) on Estrogen Receptor β (ERβ) Response to 5α-Reductase Inhibition in Prostate Epithelial Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE47354
Genome-wide expression profiling of Hic-5 and TGFB in WPMY fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Identifying the effect of the co-regulator Hic-5 (TGFB1I1) and TGFB on the transcriptional profile of WPMY human prostate fibroblast cells with view to further elucidating the broader biological role of Hic-5 and TGFB on fibroblast.

Publication Title

VDR activity is differentially affected by Hic-5 in prostate cancer and stromal cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP067022
Expression data from dexamethasone treated mouse embryonic hypothalamic progenitor/stem cells isolated from wild type C57Bl/6 male or female mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used RNA-Seq to detail the global program of sexually dimorphic dexamethasone regulated gene expression in embryonic hypothalamic neural progenitor/stem cells. Overall design: RNAseq on Primary E14.5 mouse hyothalamic neurosphere cultures. 4 conditions - Male Dex, Male EtOH, Female Dex and Female EtOH. There are 3 biological replicates for each condition and all the 12 samples are run on two lanes (techinical duplicates).

Publication Title

Research Resource: The Dexamethasone Transcriptome in Hypothalamic Embryonic Neural Stem Cells.

Sample Metadata Fields

Sex, Cell line, Treatment, Subject

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accession-icon GSE28437
Expression data from mouse small intestinal intraepithelial lymphocytes
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined.

Publication Title

Gammadelta intraepithelial lymphocytes are essential mediators of host-microbial homeostasis at the intestinal mucosal surface.

Sample Metadata Fields

Specimen part

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accession-icon GSE68756
Sox9 controls self-renewal of oncogene targeted cells and links tumor initiation and invasion
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sox9 Controls Self-Renewal of Oncogene Targeted Cells and Links Tumor Initiation and Invasion.

Sample Metadata Fields

Specimen part

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accession-icon GSE68613
Sox9 controls self-renewal of oncogene targeted cells and links tumor initiation and invasion [Affymetrix]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sox9 is a transcription factor expressed in most solid tumors. However, the molecular mechanisms underlying Sox9 function during tumorigenesis remain unclear. Here, using a genetic mouse model of basal cell carcinoma (BCC), the most frequent cancer in human, we show that Sox9 is expressed from the earliest step of tumor formation in a Wnt/-catenin dependent manner. Deletion of Sox9 together with the constitutive activation of Hedgehog (HH) signaling completely prevents BCC formation and leads to a progressive loss of oncogene expressing cells. Transcriptional profiling of oncogene expressing cells with Sox9 deletion, combined with in vivo ChIP-sequencing uncovers a cancer-specific gene network regulated by Sox9 that promotes stemness, extracellular matrix (ECM) deposition and cytoskeleton remodeling while repressing epidermal differentiation. Our study identifies the molecular mechanisms regulated by Sox9 that links tumor initiation and invasion.

Publication Title

Sox9 Controls Self-Renewal of Oncogene Targeted Cells and Links Tumor Initiation and Invasion.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE47592
5-hydroxymethylcytosine marks promoters in colon that resist hypermethylation in cancer
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

5-hydroxymethylcytosine marks promoters in colon that resist DNA hypermethylation in cancer.

Sample Metadata Fields

Sex, Specimen part, Cell line, 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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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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