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accession-icon GSE18882
Effect of cellular and viral miRNAs on target RNA half-life in three human B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Total, nascent and unlabeled RNA were prepared following 1h of labeling with 100 M 4-thiouridine and 3 replicates analyzed by Affymetrix Gene ST 1.0 arrays

Publication Title

Systematic analysis of viral and cellular microRNA targets in cells latently infected with human gamma-herpesviruses by RISC immunoprecipitation assay.

Sample Metadata Fields

Cell line

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accession-icon GSE17180
Identification of KSHV, EBV and cellular miRNA targets in human B-cells using RIP-Chip
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

RIP-Chip was performed on DG75-eGFP, DG75-10/12, BCBL-1, BL41, BL41 B95.8 and Jijoye using anti-human Ago2 (11A9) antibodies. Anti-BrdU antibodies were used as controls for DG75-eGFP, DG75-10/12 and BCBL-1. Total RNA was used as control for BL41, BL41 B95.8 and Jijoye. Samples were analyzed on Affymetrix Gene ST 1.0 Arrays (2 independent biological replicates / sample)

Publication Title

Systematic analysis of viral and cellular microRNA targets in cells latently infected with human gamma-herpesviruses by RISC immunoprecipitation assay.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16416
Expression data from human primary fibroblasts treated with Trypanosoma cruzi-conditioned medium
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The intracellular pathogen Trypanosoma cruzi secretes an activity that blocks TGF--dependent induction of connective tissue growth factor (CTGF/CCN2). Here, we address the mechanistic basis for T. cruzi-mediated interference of

Publication Title

A soluble factor from Trypanosoma cruzi inhibits transforming growth factor-ß-induced MAP kinase activation and gene expression in dermal fibroblasts.

Sample Metadata Fields

Specimen part

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accession-icon GSE64686
Expression data from the inducible expression of EWS-FLI1 (EF) in embryoid bodies
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oncogenic transformation in Ewing sarcoma tumors is driven by the fusion oncogene EWS-FLI1. The inducible expression of EWS-FLI1 (EF) in embryoid bodies, or collections of differentiating stem cells, generates cells with properties of Ewing sarcoma tumors, including characteristics of transformation. These cell lines exhibit anchorage-independent growth, a lack of contact inhibition and a strong Ewing sarcoma gene expression signature. These cells also demonstrate a requirement for the persistent expression of EWS-FLI1 for cell survival and growth.

Publication Title

Modeling the initiation of Ewing sarcoma tumorigenesis in differentiating human embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE96997
Investigating global transcript dynamics in mitotically arrested budding yeast cells
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 142 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Transcript dynamics in mitotic exit mutants in the S. cerevisiae BF264-15D strain background. We examined the extent to which periodic cell-cycle transcription persisted in cells arrested in anaphase with intermediate level of B-cyclins.

Publication Title

Reconciling conflicting models for global control of cell-cycle transcription.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17067
A quantitative model of transcription regulation reveals the role of non-conserved enhancers
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We identify sites of combinatorial control by performing high throughput ChIP experiments on p300, CREB-binding protein (CBP), the deacetylase SIRT1 and on multiple DNA-binding transcription factors in three different tissues. We present a quantitative model of transcriptional regulation that reveals the contribution of each binding site to tissue-specific gene expression in several mouse cell types. Binding to both evolutionarily conserved and non-conserved sequences is found to contribute significantly to transcriptional regulation. We demonstrate that binding location strongly predicts the expression level of nearby genes.

Publication Title

A quantitative model of transcriptional regulation reveals the influence of binding location on expression.

Sample Metadata Fields

Specimen part

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accession-icon SRP156448
The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Wnt gene family is an evolutionarily conserved group of proteins that regulate cell growth, differentiation, and stem cell self-renewal. Aberrant Wnt signaling in human breast tumors has been proposed to be an attractive drug target, especially in the basal-like subtype where canonical Wnt signaling is both enriched and predictive of poor clinical outcomes. The development of effective Wnt based therapeutics, however, has been slowed in part by a limited understanding of the context dependent nature with which these aberrations influence breast tumorigenesis. We recently reported that MMTV-Wnt1 mice, which are an established model for studying Wnt signaling in breast tumors, develop two subtypes of tumors by gene expression classification: Wnt1-EarlyEx and Wnt1-LateEx. Here, we extend this initial observation and show that Wnt1-EarlyEx tumors had high expression of canonical Wnt, non-canonical Wnt, and EGFR signaling pathway signatures. Therapeutically, Wnt1-EarlyEx tumors had a dynamic reduction in tumor volume when treated with an EGFR inhibitor. Wnt1-EarlyEx tumors also had primarily Cd49fpos/Epcamneg FACS profiles, but were unable to be serially transplanted into wild-type FVB female mice. Wnt1-LateEx tumors, conversely, had a bloody gross pathology, which was highlighted by the presence of 'blood lakes' by H&E staining. These tumors had primarily Cd49fpos/Epcampos FACS profiles, but also contained a secondary Cd49fpos/Epcamneg subpopulation. Wnt1-LateEx tumors were enriched for activating Hras1 mutations and were capable of reproducing tumors when serially transplanted into wild-type FVB female mice. This study definitely shows that the MMTV-Wnt1 mouse model produces two phenotypically distinct subtypes of mammary tumors. Importantly, these subtypes differ in their therapeutic response to an EGFR inhibitor, suggesting that a subset of human tumors with aberrant Wnt signaling may also respond to erlotinib. Overall design: Agilent gene expression microarrays were performed comparing RNA from FVB/n MMTV-Wnt1 mammary tumors to a common mouse reference sample. Agilent CGH microarrays were performed comparing DNA from FVB/n MMTV-Wnt1 mammary tumors to DNA from FVB wild-type mice. RNAseq libraries were prepared from FVB/n MMTV-Wnt1 mammary tumors using a TruSeq RNA kit before being submitted to the Lineberger Comprehensive Cancer Center Genomics Core to be run on the Illumina HiSeq 2000.

Publication Title

The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE60582
Gene expression profile of splenic CD19 cells from NTg, PTPROt Tg, TCL1 Tg and PTPROt/TCL1 double Tg mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

TCL1 is an an oncogene and transgenic (Tg) mice expressing TCL1 specifically in B-cells are well-characterized models for chronic lymphocytic leukemia. On the contrary, PTPROt is a phosphatase with tumor suppressor characteristics in many cancers including leukemia. Our hypothesis was that transgenic expression of PTPROt in the B-cells of TCL1 Tg mice will alleviate disease phenotype and allow the study of the in vivo mechanism of action of PTPROt. To test this we have generated Tg mice with B-cell specific expression of PTPROt and crossed these mice with the TCL1 Tg mice.

Publication Title

PTPROt-mediated regulation of p53/Foxm1 suppresses leukemic phenotype in a CLL mouse model.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE18854
Time course analysis of dedifferentiation in porcine follicular granulosa cells
  • organism-icon Sus scrofa
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Cellular dedifferentiation signifies the withdrawal of cells from a specific differentiated state into a stem cell-like undifferentiated state. However, the mechanism of dedifferentiation remains obscure. We showed that follicular granulosa cells (GC), which have distinct functions in vivo, can dedifferentiate during culture in vitro and acquire multipotency.

Publication Title

Dedifferentiated follicular granulosa cells derived from pig ovary can transdifferentiate into osteoblasts.

Sample Metadata Fields

Specimen part

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accession-icon GSE35830
Seminal plasma and transforming growth factor- regulate gene expression in human Ect1 ectocervical epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study we examined the influence of seminal plasma on gene expression in human Ect1 ectocervical epithelial cells, and the extent to which recombinant TGF3 elicits comparable changes. Ect1 cells were incubated with recombinant human TGF3 (5 ng/ml), 10% pooled human seminal plasma (v/v), or medium alone for 10h. RNA was reverse transcribed into cDNA and hybridized to Affymetrix GeneChip Human Genome U133 plus 2.0 microarrays (Affymetrix, Santa Clara, CA). Exposure of Ect1 cells to seminal plasma resulted in differential expression of a total of 3955 probe sets, identified using high stringency criteria with MAS 5.0 analysis. These corresponded to 1338 genes up-regulated and 1343 genes down-regulated by seminal plasma. TGF3 treatment of Ect1 cells resulted in differential expression of 884 probe sets, corresponding to 346 up-regulated genes and 229 down-regulated genes. The genes differentially regulated by seminal plasma included several genes associated with cytokinecytokine receptor interaction, TGF signalling, JAK/STAT signalling or VEGF signalling pathways, as specified by the KEGG database. Of 47 genes in these families, 17 (36.1%) were similarly regulated by both seminal plasma and TGF3. These data, together with additional experiments showing all three TGF isoforms can regulate inflammatory cytokine expression in Ect1 cells, identify TGF isoforms as key agents in seminal plasma that signal induction of pro-inflammatory cytokine synthesis in cervical cells.

Publication Title

TGF-β mediates proinflammatory seminal fluid signaling in human cervical epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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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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