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accession-icon GSE45812
Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex
  • organism-icon Mus musculus
  • sample-icon 16 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

Dicer deficiency reveals microRNAs predicted to control gene expression in the developing adrenal cortex.

Sample Metadata Fields

Specimen part

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accession-icon GSE45592
Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex [array]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

MicroRNAs (miRNAs) are small, endogenous, non-protein coding RNAs that are an important means of post-transcriptional gene regulation. Deletion of Dicer, a key miRNA processing enzyme, is embryonic lethal in mice, and tissue-specific Dicer deletion results in developmental defects. Using a conditional knockout model, we generated mice lacking Dicer in the adrenal cortex. These Dicer knockout (KO) mice exhibited perinatal mortality and failure of the adrenal cortex during late gestation between embryonic day 16.5 (E16.5) and E18.5. Further study of Dicer KO adrenals demonstrated a significant loss of Sf1 expressing cortical cells that was histologically evident as early as E16.5 coincident with an increase in p21 and cleaved-caspase 3 staining in the cortex. However, peripheral cortical proliferation persisted in KO adrenals as assessed by anti-PCNA staining. To further characterize the embryonic adrenals from Dicer KO mice, we performed microarray analyses for both gene expression and miRNA on purified RNA isolated from control and KO adrenals of E15.5 and E16.5 embryos. Consistent with the absence of Dicer and the associated loss of miRNA-mediated mRNA degradation, we observed an up-regulation of a small subset of adrenal transcripts in Dicer KO mice, most notably the transcripts coded by the genes Nr6a1 and Acvr1c. Indeed, several miRNAs, including let-7, miR-34c, and miR-21 that are predicted to target these genes for degradation, were also markedly down-regulated in Dicer KO adrenals. Together these data suggest a role for miRNA mediated regulation of a subset of genes that are essential for normal adrenal growth and homeostasis.

Publication Title

Dicer deficiency reveals microRNAs predicted to control gene expression in the developing adrenal cortex.

Sample Metadata Fields

Specimen part

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accession-icon SRP043678
Long-term survival of influenza virus infected club cells drives immunopathology
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Analysis of mRNA expression of influenza infected and uninfected pulmonary epithelial cells in vivo Overall design: Analysis of mRNA expression of influenza infected and uninfected pulmonary epithelial cells in vivo

Publication Title

Long-term survival of influenza virus infected club cells drives immunopathology.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23206
NSCLC cells treated with Gefitinib
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

About 10% of all NSCLC patients respond to gefitnib treatment and all of these patients will acquire resistance to the EGFR TKI.

Publication Title

Rapidly acquired resistance to EGFR tyrosine kinase inhibitors in NSCLC cell lines through de-repression of FGFR2 and FGFR3 expression.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE104792
Expression changes with JAK2V617F and TNF receptor block in a murine model of MPN
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We analyzed expression changes between JAK2V617F positive bone marrow cells and JAK2V617F negative cells

Publication Title

Autocrine Tnf signaling favors malignant cells in myelofibrosis in a Tnfr2-dependent fashion.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE33371
Beta-catenin status effects in human adrenocortical carcinomas (33), adenomas (22), and normal adrenal cortex (10)
  • organism-icon Homo sapiens
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We scored adrenocortical carcinomas and adenomas for abnormal beta-catenin staining, and sequenced the beta-catenin gene in some samples. We compared adrenocortincal carcinomas with and without abnormal beta-catenin staining and found many significant expression differences and significant results from enrichment testing. A similar comparison in the adenomas gave relatively few differences, and they did not correlate to differences found for the carcinomas. Abnormal beta-catenin staining was associated with mitotic rate and poorer patient survival in the carcinomas. In a second independent data set (given in a supplement) we again found beta-catenin associated with poor survival. The array data given is the same as GEO series GSE10927, with additional characteristics about beta-catenin, and new patient followup data. The analysis shown in a supplementary Excel file is also new.

Publication Title

Progression to adrenocortical tumorigenesis in mice and humans through insulin-like growth factor 2 and β-catenin.

Sample Metadata Fields

Sex, Age

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accession-icon GSE57613
Hypoxia regulates alternative splicing of HIF and non-HIF target genes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Human Exon 1.0 ST Array (huex10st)

Description

Alternative RNA splicing analysis in Hep3B cell cultured under 21% (N1,3,5) or 1.2% (H2,4,6) oxygen

Publication Title

Hypoxia regulates alternative splicing of HIF and non-HIF target genes.

Sample Metadata Fields

Cell line

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accession-icon SRP194241
Single cell analysis of human fetal liver captures the transcriptional profile of hepatobiliary hybrid progenitors
  • organism-icon Homo sapiens
  • sample-icon 492 Downloadable Samples
  • Technology Badge Icon

Description

The liver parenchyma is composed of hepatocytes and bile duct epithelial cells (BECs). Controversy exists regarding the cellular origin of human liver parenchymal tissue generation during embryonic development, homeostasis or repair. Here we report the existence of a hepatobiliary hybrid progenitor (HHyP) population in human fetal liver using single-cell RNA sequencing. HHyPs are anatomically restricted to the ductal plate of fetal liver and maintain a unique transcriptional profile distinct from fetal hepatocytes, mature hepatocytes and mature BECs. In addition, molecular heterogenicity within the EpCAM+ population of freshly isolated fetal and adult human liver reveals diverse gene expression signatures of hepatic and biliary lineage potential. Finally, we FACS isolated fetal HHyPs and confirmed their hybrid progenitor phenotype in vivo. Our study suggests that hepatobiliary progenitor cells previously identified in mice also exist in humans, and can be distinguished from other parenchymal populations, including mature BECs, by distinct gene expression profiles. Overall design: Primary samples from 5 2nd trimester human fetal livers and 3 uninjured adult human livers for single cell RNA sequencing by Smartseq2.

Publication Title

Single cell analysis of human foetal liver captures the transcriptional profile of hepatobiliary hybrid progenitors.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE19246
A novel method of amplification of FFPET derived-RNA enables accurate disease classification with microarrays
  • organism-icon Homo sapiens
  • sample-icon 171 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A new method for amplification and labeling of RNA is assessed that permits gene expression microarray analysis of formalin-fixed paraffin embedded tissue (i.e. FFPET) samples.

Publication Title

A novel method of amplification of FFPET-derived RNA enables accurate disease classification with microarrays.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE7896
S1P mediates key targets associated with survival, proliferation and pluripotency in human embryonic stem cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human embryonic stem cells (hESCs) replicate by the process of self-renewal, whilst maintaining their pluripotency. Understanding the pathways involved in the regulation of this self-renewal process will assist in developing fully-defined conditions for the proliferation of hESCS required for therapeutic applications. We previously demonstrated a role for Sphingosine-1-phosphate (S1P) in the survival and proliferation of hESCs. The present study investigates further key signalling pathways and the downstream targets of S1P.

Publication Title

Sphingosine-1-phosphate mediates transcriptional regulation of key targets associated with survival, proliferation, and pluripotency in human embryonic stem cells.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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