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accession-icon SRP061931
Expression profiling of fetal mammary cells that express ectopic levels of Sox10
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We use RNA-sequencing to generate gene expression profiles of fetal mammary cells that have been induced to overexpress Sox10. These data highlight multiple important molecular mechanisms that are altered in response to this perturbation, and offer a resource to probe the basis of the stem/progenitor and EMT-like functions that are mediated by Sox10 in mammary cells. Overall design: Expression profiling of fetal mammary cells that express ectopic levels of Sox10

Publication Title

Sox10 Regulates Stem/Progenitor and Mesenchymal Cell States in Mammary Epithelial Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP061930
Expression profiling of fetal mammary cells
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We use RNA-sequencing to generate gene expression profiles of fetal mammary cells with unique sorting strategies. These analyses reveal that sorting fetal mammary cells with Sox10 and EpCAM sorting markers provides a stroma-free fMaSC-enriched cell population. The gene expression profiling of these cells offers a resources to probe the molecular mechanisms that specify this unique cell state. Overall design: Examination of 2 different sorting strategies for fetal mammary cells

Publication Title

Sox10 Regulates Stem/Progenitor and Mesenchymal Cell States in Mammary Epithelial Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP171158
Mutationally-activated PI3'-kinase-a promotes de-differentiation of lung tumors initiated by the BRAFV600E oncoprotein kinase
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Human lung adenocarcinoma exhibits a propensity for de-differentiation, which complicates diagnosis and treatment, and predicts for poor overall patient survival. In genetically engineered mouse (GEM) models of lung cancer, expression of the BRAFV600E oncoprotein kinase initiates the growth of benign tumors that retain characteristics of their cell of origin, alveolar type II (ATII) pneumocytes. Cooperating genetic alterations such as silencing of the PTEN tumor suppressor or expression of mutationally-activated PI3-kinase-a (PIK3CAH1047R) promote malignant progression of such benign tumors to malignant adenocarcinoma, though their effects on differentiation status are unknown. To address this in vivo, we generated a new conditional BrafCAT allele in which Cre-mediated recombination leads to expression of a bi-cistronic mRNA encoding both BRAFV600E and the tdTomato fluorescent protein. Using this model, we demonstrate that coincident expression of BRAFV600E and PIK3CAH1047R in ATII pneumocytes leads to rapid and widespread cell de-differentiation. Surprisingly, the combined effects of BRAFV600E and PIK3CAH1047R on ATII pneumocyte identity occurred without loss of expression of the lung lineage transcription factors NKX2.1, FOXA1, or FOXA2. Instead, we demonstrate a novel role of PGC1a in maintaining pneumocyte identity, which is lost upon PIK3CAH1047R expression. These findings provide additional insight into how two of the most commonly mutated growth factor signaling pathways contribute to the pathogenesis of lung adenocarcinoma. Overall design: BRAFV600E mutant mouse lung adenocarcinoma (n=6) vs BRAFV600E;PIK3CAH1047R mutant lung adenocarcinoma (n= 8), and BRAFV600E;PGC1aHET (n=5) vs BRAFV600E;PGC1aNULL tumors (n=4)

Publication Title

Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAF<sup>V600E</sup> oncoprotein kinase.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE15141
EGR1 regulates metastatic potential of v-src transformed chicken sarcoma cell lines
  • organism-icon Gallus gallus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

A model of tumor metastasis based on v-src transformed immortalized cell lines was developed. The model consists of highly metastatic PR9692 cell line and a derived clone PR9692-E9 which has lost the metastatic abilities. Introduction of exogenous EGR1 gene into the non-metastasizing PR9692-E9 cells completely restores the metastatic potential. Revealed changes in gene expression provide insight into the molecular mechanisms contolling metastatic behavior of sarcoma cells.

Publication Title

The transcription factor EGR1 regulates metastatic potential of v-src transformed sarcoma cells.

Sample Metadata Fields

Cell line

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accession-icon GSE42516
Downregulation of the HOPX gene decreases metastatic activity in a chicken sarcoma cell line model and identifies genes associated with metastasis
  • organism-icon Gallus gallus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

Metastatic progression is the leading cause of cancer mortality yet we have an incomplete view of the genetic events governing this process. An investigation was undertaken to explore the role of homeodemain only protein X (HOPX) in metastatic propensity and to identify other genes that may participate in metastasis development. The transcription factor HOPX was assessed for its possible involvement in metastasis formation using a knock-down induced by plasmid-delivered shRNAs. We used our original model system of chicken v-src-transformed tumour cell line PR9692 and its subclone (PR9692-E9) that have lost the ability to induce metastases after inoculation into syngeneic chickens without any significant change in primary tumour formation. We found that also a PR9692 cell line with decreased expression of HOPX gene (PR9692-shHOPX) lost its metastatic capacity in vivo (in chickens) and displayed a reduced cell migration in vitro. We compared the gene expression profiles of control (PR9692-shMOCK) and PR9692-shHOPX cells using oligonucleotide microarrays, assuming that genes with differential expression might be associated with metastasis. The data were compared with a previous study showing differences in gene expression between the PR9692 and PR9692-E9 cells. Bioinformatics was applied to identify gene expression patterns associated with metastasis. 234 genes were identified to show at least 2-fold change in both pairs of cell lines. The results were validated with real-time quantitative RT-PCR and the differential expression was confirmed for several genes. We were also able to demonstrate a significant change at protein level in case of three selected genes (NCAM, FOXG1, ITGA4). shRNA mediated knockdown of one of the identified HOPX regulated genes (integrin alpha 4) in the PR9692 cell line itself showed a marked inhibition of metastasis formation.

Publication Title

Downregulation of HOPX controls metastatic behavior in sarcoma cells and identifies genes associated with metastasis.

Sample Metadata Fields

Cell line

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accession-icon GSE4737
HCaRG vs NEO
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Summary:

Publication Title

HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2555
HCaRG-9 vs NEO-1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A Array (hgu133a)

Description

HEK293 cells were transfected with control plasmid (pcDNAI/Neo;Invitrogen) or with the plasmid encoding HCaRG. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen).

Publication Title

HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE74659
SCL and LMO1 reprogram thymocytes into self-renewing cells.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The SCL and LMO1 oncogenic transcription factors reprogram thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Here we report that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1.

Publication Title

SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE71663
Profiling of Brat associated mRNAs from Drosophila embryos by RIP-CHIP
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.1 ST Array (drogene11st)

Description

The Drosophila TRIM-NHL protein Brain tumor (Brat) plays important roles during early embryogenesis, in cell fate decisions, during neurogenesis and in mature neurons. Brat is an RNA-binding protein and functions as translational repressor. However, which RNAs Brat regulates and how RNA-binding specificity is achieved, is unknown. Using RNA-Immunoprecipitation we identify Brat-bound mRNAs in Drosophila embryos and define a consensus binding motif.

Publication Title

The Crystal Structure of the NHL Domain in Complex with RNA Reveals the Molecular Basis of Drosophila Brain-Tumor-Mediated Gene Regulation.

Sample Metadata Fields

Specimen part

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accession-icon SRP074247
Global Profiling of the Cellular Alternative RNA Splicing Landscape During Virus-host Interactions
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Background Alternative splicing (AS) is a central mechanism of genetic regulation which modifies the sequence of RNA transcripts in higher eukaryotes. AS has been shown to increase both the variability and diversity of the cellular proteome by changing the composition of resulting proteins through differential choice of exons to be included in mature mRNAs. Results In the present study, alterations to the global RNA splicing landscape of cellular genes upon viral infection were investigated through high-throughput RNA sequencing (RNA-seq) studies using mammalian reovirus as a model. Our study provides the first comprehensive portrait of global changes in the RNA splicing signatures that occur in eukaryotic cells following infection with a human virus. We identify modifications in the AS patterns of 240 cellular transcripts frequently involved in the regulation of gene expression and RNA metabolism. A significant number of the modified transcripts are also encoded by genes with important roles in viral infection/immunity. These modifications are expected to alter the functions of many cellular proteins. Finally, we used RT-PCR analysis in order to experimentally validate differential modifications in alternative splicing patterns that were observed through RNA-seq studies. Conclusion The present study demonstrated that viral infection can extensively modify the splicing patterns of numerous cellular transcripts. These findings provide additional insights into the complexity of virus-host interactions as these splice variants expand proteome diversity and function during viral infection. Finally, these data open new avenues of research for a better understanding of post-transcriptional events during virus infection and possible new targets toward the development of antiviral agents. Overall design: mRNAs were isolated from L929 mouse cell line, 14 hours after infection with T3D-S Reovirus or T3D-S Mutant reovirus at a MOI of 50. Control cells were uninfected. The resulting libraries were multiplexed and paired-end sequenced using Illumina HiSeq. Gene expression and alternative splicing were caracterized using Bowtie and RSEM.

Publication Title

Global Profiling of the Cellular Alternative RNA Splicing Landscape during Virus-Host Interactions.

Sample Metadata Fields

Specimen part, Cell line, 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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