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accession-icon SRP188245
CDKN2A-specific probe captured RNA-sequencing (RNACap-Seq) (HEK293T MCF7)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The CDKN2A/B locus at 9p21.3 contains crucial tumor suppressors (P16, P14, and P15) and oncogenic lncRNA ANRIL genes. This locus is most frequently inactivated in cancer genomes by deletion and DNA methylation. However, the mechanisms coordinately regulating their expression level are far from clear. In the present study, a novel lncRNA, P14AS, was characterized in the antisense strand of the fragment near CDKN2A in human cell lines using CDKN2A-specific probe captured RNA-sequencing (RNACap-Seq). Overall design: RNAs were characterized in the antisense strand of the fragment near CDKN2A in human cell lines using CDKN2A-specific probe captured RNA-sequencing (RNACap-Seq).

Publication Title

Characterization of novel LncRNA P14AS as a protector of ANRIL through AUF1 binding in human cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE15872
Dynamic patterning at the pylorus: formation of an epithelial intestine-stomach boundary in late fetal life
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In the adult mouse, distinct morphological and transcriptional differences separate stomach from intestinal epithelium. Remarkably, the epithelial boundary between these two organs is literally one cell thick. This discrete junction is established suddenly and precisely at embryonic day (E) 16.5, by sharpening a previously diffuse intermediate zone. In the present study, we define the dynamic transcriptome of stomach, pylorus and intestinal tissues between E14.5 and E16.5. We show that establishment of this boundary is concomitant with the induction of over a thousand genes in intestinal epithelium, and these gene products provide intestinal character. Hence, we call this process intestinalization. We identify specific transcription factors (Hnf4g, Creb3l3 and Tcfec) and examine signaling pathways (Hedgehog and Wnt) that may play a role in this process. Finally, we define a unique expression domain at the pylorus itself and detect novel pylorus-specific patterns for the transcription factor Gata3 and the secreted protein nephrocan.

Publication Title

Dynamic patterning at the pylorus: formation of an epithelial intestine-stomach boundary in late fetal life.

Sample Metadata Fields

Specimen part

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accession-icon GSE14247
Interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 triggers ethylene responses in Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

A complex interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 is essential for triggering ethylene responses in plants.

Publication Title

Interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 triggers ethylene responses in Arabidopsis.

Sample Metadata Fields

Age, Treatment

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accession-icon SRP005103
Deep sequencing analysis of the murine transcriptome response to different virulent parenthood B. melitensis infection
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

In this study, we employed the Illumina Genome Analyzer platform to perform a Digital Gene Expression (DGE) analysis of the peritoneal macrophages genome-wide transcriptome response to B.melitensis infection. Common changes in gene expression were observed among Brucella app. infected macrophages suggesting similar strategies were employed for their survival and replication, inducing anti-inflammatory and anti-apoptotic. A total of 1019 differentially expressed (DE) transcripts were identified in the macrophages 4 hours after differ virluent B.melitensis infection, especially genes participated lysosome pathway and MAPK pathway. Our findings demonstrate previously unrecognized changes in gene transcription that are associated with B.melitensis infection in the macrophages, and many significant pathways (cascades) identified in the study clearly merit further investigation. Our data provide new clues to understand the molecular attenuation mechanism of M5-90 and a firm foundation for reducing vaccine residual virulence, enhancing vaccine efficacy. Overall design: Examination oftwo peritoneal macrophages infected brucella and one blank control.

Publication Title

Deep-sequencing analysis of the mouse transcriptome response to infection with Brucella melitensis strains of differing virulence.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71977
Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE71915
Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression [microarray]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer

Description

Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNFalpha can facilitate tumor progression and metastasis. However, our knowledge of the molecular mechanisms underlying TNBC progression mediated by inflammation is still limited. Here, we define the AP-1 transcription factor c-Jun cistrome, which is comprised of 13800 binding sites responsive to TNFalpha-induced signaling in TNBC cells. In addition, we show that c-Jun regulates nearly a third of the TNFalpha-elicited transcriptome. Expression of the c-Jun-regulated pro-invasion gene program is strongly associated with clinical outcomes in TNBCs. Mechanistically, we demonstrate that c-Jun drives TNFalpha-mediated TNBC tumorigenicity by transcriptional regulation of Ninj1. As exemplified by the c-Jun bound CXC chemokine genes clustered on chromosome 4, we demonstrate that NF-kB might be a pioneer factor and is required for the regulation of TNFalpha-inducible inflammatory genes, whereas c-Jun has little effect. Together, our results uncover AP-1 as an important determinant for inflammation-induced cancer progression, rather than inflammatory response.

Publication Title

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE4043
Gene profiling analysis of Src chemical rescue
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The restoration of catalytic activity to mutant enzymes by small molecules is well-established for in vitro systems. Here we show that the protein tyrosine kinase Src R388A mutant can be rescued in live cells using the small molecule imidazole. Cellular rescue of a v-Src homolog was rapid and reversible and conferred predicted oncogenic properties. Using chemical rescue in combination with mass spectrometry, six known Src kinase substrates were confirmed, and several new protein targets identified. Chemical rescue data suggests that c-Src is active under basal conditions. Rescue of R388A c-Src also allowed contributions of Src to the MAP kinase pathway to be clarified. This chemical rescue approach is likely to be of broad utility in cell signaling.

Publication Title

Chemical rescue of a mutant enzyme in living cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP056076
RNA-seq analysis of gene expression patterns responding to TSA treatment during hESC neural differentiation
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the differential roles of an HDAC inhibitor-TSA during hESC nerual commitment. In the initiation of hESC differentiation, TSA could inhibit the downregulation of pluripotency genes to maintain pluripotency, whereas in the neural commitment stage, TSA could promote neural gene expression to assist hESC nerual determination. Overall design: Examination of gene expression patterns in hESCs, day 4 or day 8 differentiated cells without or with TSA treatment

Publication Title

Dual roles of histone H3 lysine 9 acetylation in human embryonic stem cell pluripotency and neural differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP079214
RNAseq to profile IFNg response in human primary monocytes
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We did transcriptome profiling for monocytes treated with or without IFNg to characterize IFNg response. Overall design: Human primary monocytes were cultured for 24 hours with or without IFNg, harversted and prepared for RNA for RNAseq.

Publication Title

IFN-γ Induces Histone 3 Lysine 27 Trimethylation in a Small Subset of Promoters to Stably Silence Gene Expression in Human Macrophages.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP186005
Measuring the influence of RNA binding proteins on A-to-I RNA editing in the Drosophila brain
  • organism-icon Drosophila melanogaster
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

A-to-I RNA editing levels differ across tissues and cell types, but regulators of the editing process are largely unknown. We used RNA-seq on whole fly brains with different RNA binding proteins knocked down to test for A-to-I RNA editing level differences between controls and knockdowns. Overall design: To screen for editing regulators in the Drosophila brain, we crossed a pan-neuronal Gal4 driver, C155-Gal4, to different UAS-shRNA lines targeting individual RNA binding proteins, extracted RNA and made RNA-seq libraries. We sequenced four total replicates of shGFP controls and two replicates of all RNA binding protein knockdowns.

Publication Title

Zinc Finger RNA-Binding Protein Zn72D Regulates ADAR-Mediated RNA Editing in Neurons.

Sample Metadata Fields

Sex, Specimen part, 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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