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accession-icon GSE71053
Differential Effect of Surgical Manipulation on Gene Expression in Normal Breast Tissue and Breast Tumour Tissue
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling is a promising diagnostic and prognostic tool. Expression profiles are snap-shots of mRNA levels at time of extraction and they have been shown to be affected by tissue handling during sample collection. The effect of cold (room temperature) ischemia in the time interval between surgical removal of the specimen and freezing has been described in a number of studies. However, not much is known about the effect of warm (body temperature) ischemia during surgery.

Publication Title

Differential effect of surgical manipulation on gene expression in normal breast tissue and breast tumor tissue.

Sample Metadata Fields

Sex, Specimen part, Disease, Subject

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accession-icon GSE147231
Identification of human cytotoxic ILC3s
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Pico Assay HT (clariomshumanht)

Description

Human ILCs are classically categorized into five subsets; cytotoxic CD127-CD94+ NK cells and non-cytotoxic CD127+CD94-, ILC1s, ILC2s, ILC3s and LTi cells. Here, we identify a novel subset within the CD127+ ILC population, characterized by the expression of the cytotoxic marker CD94. These CD94+ ILCs strongly resemble conventional ILC3s in terms of phenotype, transcriptome and cytokine production, but are highly cytotoxic. IL-15 was unable to induce differentiation of CD94+ ILCs towards mature NK cells. Instead, CD94+ ILCs retained RORγt, CD127 and CD200R expression and produced IL-22 in response to IL-15. Culturing non-cytotoxic CD127+ ILC1s or ILC3s with IL-12 induced upregulation of CD94 and cytotoxic activity, effects that were not observed with IL-15 stimulation. Thus, human helper ILCs can acquire a cytotoxic program without differentiating into NK cells.

Publication Title

Identification of human cytotoxic ILC3s.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP027535
Targeting H3K4 methylation as a therapeutic strategy for Huntington''s disease (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2000

Description

Transcriptional dysregulation is an early feature of Huntington''s disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD. Overall design: mRNA-seq in wild type and R6/2 cortex and striatum at 8 and 12 weeks.

Publication Title

Targeting H3K4 trimethylation in Huntington disease.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE15617
Uncovering the Arabidopsis thaliana nectary transcriptome: nectary and reference tissues
  • organism-icon Arabidopsis thaliana
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Many flowering plants attract pollinators by offering a reward of floral nectar. Remarkably, the molecular events involved in the development of nectaries, the organs that produce nectar, as well as the synthesis and secretion of nectar itself, are poorly understood. Indeed, to date, no genes have been shown to directly affect the de novo production or quality of floral nectar. To address this gap in knowledge, the ATH1 Affymetrix GeneChip array was used to systematically investigate the Arabidopsis nectary transcriptome to identify genes and pathways potentially involved in nectar production. In this study, we identified a large number of genes differentially expressed between secretory lateral nectaries and non-secretory median nectary tissues, as well as between mature lateral nectaries (post-anthessis) and immature lateral nectary tissue (pre-anthesis).

Publication Title

Uncovering the Arabidopsis thaliana nectary transcriptome: investigation of differential gene expression in floral nectariferous tissues.

Sample Metadata Fields

Specimen part

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accession-icon GSE15601
Uncovering the Arabidopsis thaliana nectary transcriptome
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Many flowering plants attract pollinators by offering a reward of floral nectar. Remarkably, the molecular events involved in the development of nectaries, the organs that produce nectar, as well as the synthesis and secretion of nectar itself, are poorly understood. Indeed, to date, no genes have been shown to directly affect the de novo production or quality of floral nectar. To address this gap in knowledge, the ATH1 Affymetrix GeneChip array was used to systematically investigate the Arabidopsis nectary transcriptome to identify genes and pathways potentially involved in nectar production. In this study, we identified a large number of genes differentially expressed between secretory lateral nectaries and non-secretory median nectary tissues, as well as between mature lateral nectaries (post-anthessis) and immature lateral nectary tissue (pre-anthesis).

Publication Title

Uncovering the Arabidopsis thaliana nectary transcriptome: investigation of differential gene expression in floral nectariferous tissues.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE10516
Identification of genes controlled by LMX1B in the developing mouse hindlimb bud
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in e11.5 mouse proximal limb tissue lacking the Lmx1b gene. Because Lmx1b is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning.

Publication Title

Identification of genes controlled by LMX1B in the developing mouse limb bud.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP098580
RNA-seq analysis of gene expression in adult head of Canton-S and Bully lines
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Goal: Identify genes that are differentially expressed in hyper-aggressive Bully line. We used wildtype Canton-S flies as control. We also explored the effect of developmental temperature on gene expression. Overall design: Total RNA were extracted from 6-day-old adult heads from Canton-S or Bully lines that were raised at 19C or 25C. A total of 4 samples were obtained. For each sample, 2 independent biological replicates were included.

Publication Title

Putative transmembrane transporter modulates higher-level aggression in <i>Drosophila</i>.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon SRP069872
Uncoupling X chromosome number from sex determination separates contribution of sex and X dose to sex-biased gene expression in C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages. Overall design: RNA-Seq profiles of C. elegans XO hermaphrodite and XX male L3 larvae and adults

Publication Title

Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP044608
TNFa Signaling Exposes Latent Estrogen Receptor Binding Sites in Breast Cancer Cells [GRO-seq]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNFa, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ERa), the pioneer factor FoxA1 and the p65 subunit of the NF-?B transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNFa signaling at the gene level is also evident in the patterns of ERa and NF-?B binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ERa binding sites is predetermined prior to estrogen treatment, whereas ERa binding sites gained upon co-treatment with TNFa require NF-?B and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNFa signaling recruits FoxA1 and NF-?B to latent ERa enhancer locations and directly impact ERa enhancer accessibility. Binding of ERa to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer. Overall design: Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFa or both E2+TNFa.

Publication Title

TNFα signaling exposes latent estrogen receptor binding sites to alter the breast cancer cell transcriptome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE47937
Gene expression changes due to influenza virus induced miRNAs
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells.

Publication Title

Small RNA profiling of influenza A virus-infected cells identifies miR-449b as a regulator of histone deacetylase 1 and interferon beta.

Sample Metadata Fields

Cell line

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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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