refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 1125 results
Sort by

Filters

Technology

Platform

accession-icon SRP150723
Effect of BMP inhibition or stimulation of primary human keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

BMP treatment induces expression of late differenitation genes in primary human keratinocytes. Overall design: RNA-seq analysis after treatment with EGFR inhibitor AG1478 with or without BMP27 or BMP inhibitor DMH1. each treatment and control was performed in triplicate

Publication Title

Single-Cell ID-seq Reveals Dynamic BMP Pathway Activation Upstream of the MAF/MAFB-Program in Epidermal Differentiation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP147553
Splicing and epigenetic factors jointly regulate epidermal differentiation
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the effects of silencing SRSF1 or ZMAT2 in human epidermal stem cells on the transcriptome of epidermal stem cells. We found that silencing ZMAT2 or SRSF1 affects global splicing, however, ZMAT2 seems to regulate splicing of a smaller more specific subset of genes. Overall design: RNA-sequencing data following silencing SRSF1 or ZMAT2

Publication Title

Splicing and Chromatin Factors Jointly Regulate Epidermal Differentiation.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon SRP155035
STVI-120 Induction of differentiation in human epidermal stem cells followed by differential splicing analysis
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the effects of induction of differentiation in human epidermal stem cells on the splicing of the transcriptome. Overall design: RNA-sequencing data following induction of differentiation in human epidermal stem cells

Publication Title

Splicing and Chromatin Factors Jointly Regulate Epidermal Differentiation.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE15108
Transcription profile of fission yeast
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Wild-type cells were cultured at 30 deg and cells were harvested. Total RNAs were purified from 3 populations.

Publication Title

Mapping of long-range associations throughout the fission yeast genome reveals global genome organization linked to transcriptional regulation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE52115
Gene expression profile in peritoneal macrophage infected with Listeria monocytogenes
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Several Toll-like receptors are activated by Listeria monocytogenes infection, resulting in the activation of MyD88 dependent signaling pathway. However, the negative role of MyD88 in gene expresson is unclear.

Publication Title

Beneficial innate signaling interference for antibacterial responses by a Toll-like receptor-mediated enhancement of the MKP-IRF3 axis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP106148
p63 controls the enhancer landscape during keratinocyte differentiation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Here we characterized the transcriptome and epigenome of control keratinocytes during differentiation. Epigenomic analyses showed that the temporal enrichment of p63 motifs in dynamic enhancers underscores the key role of p63 in orchestrating the enhancer landscape during keratinocyte differentiation. The cooperation between p63 and its co-regulating factors, such as RUNX1, is important for the finetuning of gene expression. Overall design: RNA-Seq, H3K4me3 ChIP-Seq and H3K27me3 ChIP-Seq of keratinocytes during differentiation on day0(proliferation), day2(early differentiation), day4(mid differentiation) and day7(late differentiation). RUNX1 ChIP-Seq of keratinocytes at the proliferation stage(day0).

Publication Title

Mutant p63 Affects Epidermal Cell Identity through Rewiring the Enhancer Landscape.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP015845
Next Generation Sequencing Facilitates Quantitative Analysis of Argonaute 2 (Ago2)-immunoprecipitation (IP) after miR-195 or miR-497 overexpression in HepG2
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

To explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Identification of miR-195 and miR-497 target genes by sequencing Ago2-binding mRNAs and total mRNAs of miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell. Overall design: Deep sequencing of RNAs in Ago2-IP fraction and mRNAs extracted from miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell.

Publication Title

The tumor-suppressive miR-497-195 cluster targets multiple cell-cycle regulators in hepatocellular carcinoma.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

View Samples
accession-icon GSE17812
Gene expression profiling from memory P14 T cells with control or mutated ThPOK
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We noticed that ThPOK repression is readily abrogated upon in vitro TCR stimulation of peripheral CD8 T cells. This observation prompted us to investigate a role of ThPOK in the CD8 T cell response to an acute viral infection. We observed that clonal expansion is significantly less in both primary and secondary CD8 T cell responses in the absence of functional ThPOK. To approach this mechanism, we carried out a microarray analysis for comparison of gene expression between ThPOKhd/hd and ThPOKwt/wt P14 memory T cells.

Publication Title

ThPOK derepression is required for robust CD8 T cell responses to viral infection.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP161680
Identification of human gene expression induced by 4MU-xyloside treatment
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

The Golgi stress response is a homeostatic mechanism that augments the functional capacity of the Golgi apparatus when Golgi function becomes insufficient (Golgi stress). Three response pathways of the Golgi stress response have been identified in mammalian cells, the TFE3, HSP47 and CREB3 pathways, which augment the capacity of specific Golgi functions such as N-glycosylation, anti-apoptotic activity and pro-apoptotic activity, respectively. On the contrary, glycosylation of proteoglycans (PGs) is another important function of the Golgi, although the response pathway upregulating expression of glycosylation enzymes for PGs in response to Golgi stress remains unknown. Here, we found that expression of glycosylation enzymes for PGs was induced upon insufficiency of PG glycosylation capacity in the Golgi (PG-Golgi stress), and that transcriptional induction of genes encoding glycosylation enzymes for PGs was independent of the known Golgi stress response pathways and ER stress response. Promoter analyses of genes encoding these glycosylation enzymes revealed the novel enhancer element PGSE, which regulates their transcriptional induction upon PG-Golgi stress. From these observations, the response pathway we discovered is a novel Golgi stress response pathway, which we have named the PG pathway. Overall design: Three control samples (DMSO-treated) and three 4MU-xyloside-treated samples

Publication Title

PGSE Is a Novel Enhancer Regulating the Proteoglycan Pathway of the Mammalian Golgi Stress Response.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon GSE13589
Gene expression of E. coli MG1655 pOX38Km at the outside and inside of biofilms
  • organism-icon Escherichia coli
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Gene expression changes between outside and inside of biofilms were investigated. The gene expression was compared between the outside and inside of the biofilms. At the same time, the gene expressions were also compared with exponential phase and stationary phase in planktonic cells. The gene expression analysis showed that the physiological activities were higher at the outside of the biofilms than those at the inside of the biofilms. The genes induced at the ouside of the biofilms included genes involved in the stress responses and adhesions.

Publication Title

Localized expression profiles of rpoS in Escherichia coli biofilms.

Sample Metadata Fields

No sample metadata fields

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact