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accession-icon SRP007885
CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. Overall design: CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.

Publication Title

CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.

Alternate Accession IDs

GSE31486

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE51262
H3K9 Trimethylation Silences Fas Expression to Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

We have determined that verticillin A is a histone methyltransfease inhibitor that selectively inhibits human SUV39H1, SUV39H2, G9a and GLP to inhibit H3K9 methylation in human colon cancer cells. The objective here is to identify verticillin A target genes in human colon cancer cells.

Publication Title

H3K9 Trimethylation Silences Fas Expression To Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance.

Alternate Accession IDs

E-GEOD-51262

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon SRP072214
Converting adult pancreatic a-cells into ß-cells by targeting Dnmt1 and Arx
  • organism-icon Mus musculus
  • sample-icon 182 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

After their destruction in adult mice, insulin-producing pancreatic beta-cells slowly regenerate from other islet cells, like glucagon-producing alpha-cells. However the molecular basis of this conversion is unknown. Moreover it remains unclear if this intra-islet cell conversion is relevant to human diseases with extensive beta-cell loss, like in type 1 diabetes (T1D). Here, we show that subsets of glucagon-expressing cells in subjects with T1D produce Insulin and other molecular features of beta-cells, accompanied by loss of the alpha-cell regulators DNA methyltransferase 1 (Dnmt1) and Aristaless-related homeobox (Arx). We generated mice permitting lineage tracing and inactivation of Dnmt1 and Arx in adult alpha-cells. Within 3 months of Dnmt1 and Arx loss, 50% of alpha-cells converted into cells producing insulin protein but not glucagon, changes not observed in alpha-cells after only Arx or Dnmt1 loss. Single cell isolation and high-throughput RNA sequencing revealed efficient and extensive alpha-cell conversion into progeny indistinguishable by global gene expression from native beta-cells. Our work reveals pathways regulated by Arx and Dnmt1 sufficient for achieving targeted generation of beta-cells from adult pancreatic alpha-cells. Overall design: Single-cell RNA-seq of in-vivo conversion of pancreatic a-cells into ß-cells

Publication Title

Converting Adult Pancreatic Islet α Cells into β Cells by Targeting Both Dnmt1 and Arx.

Alternate Accession IDs

GSE79457

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE50994
Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Silymarin (SM) is a popular botanical medicine with purported liver protective effects. SM displays multiple effects in animal models and in cell culture including prevention of liver disease, reduction of inflammation, oxidative stress, and proliferation. Despite a plethora of data indicating that SM impinges on multiple cellular signaling pathways important in inflammation and disease, no unifying mechanisms have been forwarded. To define how SM elicits so many biological effects, the current study presents the first comprehensive transcriptional profiling study of human hepatoma cells treated with SM. The intention of the study was to focus on the early transcriptional events that are associated with SM-induced inhibition of proliferation and inflammation. Collectively, the data demonstrate that SM causes a rapid transcriptional reprogramming of cells that initially manifests as energy stress and slowing of cellular metabolism, leading to inhibition of cell growth and inflammation.

Publication Title

Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling.

Alternate Accession IDs

E-GEOD-50994

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

View Samples
accession-icon SRP163661
Differential expression of genes in fibroblasts and epithelial cells infected with dsDNA viruses
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We studied changes in a whole transcriptome during dsDNA virus infection. Overall design: Fibroblasts (MRC5 & HFF) and epithelial cells (ARPE19) were infected with HCMV, HSV1 or Ad5 and total RNA was isolated at 48, 9, or 24 hpi, respectively. Total 15 treatments were used. There were 2 biological replicates analyzed per each treatment.

Publication Title

A tumor-specific endogenous repetitive element is induced by herpesviruses.

Alternate Accession IDs

GSE120891

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP163660
Differential expression of genes in AD169-infected MRC5.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We studied changes in a whole transcriptome during HCMV infection. Overall design: Fibroblasts (MRC5) were infected with HCMV and total RNA was isolated at 48. Total 2 individual samples were used. There were 3 replicates analyzed per individual sample.

Publication Title

A tumor-specific endogenous repetitive element is induced by herpesviruses.

Alternate Accession IDs

GSE120890

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP158666
Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex
  • organism-icon Mus musculus
  • sample-icon 2756 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

During cortical development, distinct subtypes of glutamatergic neurons are sequentially born and differentiate from dynamic populations of progenitors. How progenitors and their daughter cells are temporally patterned remains unknown. Here, we trace the transcriptional trajectories of successive generations of apical progenitors (APs) and isochronic cohorts of their daughter neurons in the developing mouse neocortex using high temporal resolution parallel single-cell RNA sequencing. We identify and functionally characterize a core set of evolutionarily-conserved temporally patterned genes which drive APs from internally-driven states to more exteroceptive states, revealing a progressively increasing role for extracellular signals as corticogenesis unfolds. These embryonic age-dependent AP molecular states are reflected in their neuronal progeny as successive ground states, onto which essentially conserved early post-mitotic differentiation programs are applied. Thus, temporally unfolding molecular birthmarks present in progenitors act in their post-mitotic progeny as seeds for adult neuronal diversity. Overall design: Investigation of the transcriptional dynamics in time-locked cohorts of cortical cells across embryonic neurogenesis. Flashtag is injected at 4 ages (E12, E13, E14, E15), and cells collected 1H, 24H, 96H after birth (= a total of 12 conditions) and analyzed by single cell transcriptomics.

Publication Title

Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex.

Alternate Accession IDs

GSE118953

Sample Metadata Fields

Subject

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accession-icon GSE76109
HDAC inhibition, dopamine and long-term fear inhibition
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction.

Alternate Accession IDs

E-GEOD-76109

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE76103
HDAC inhibition, dopamine and long-term fear inhibition [mPFC data set]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Extinction-based exposure therapy is used in treating anxiety- and trauma-related disorders, however there is the need to improve its limited efficacy in individuals with impaired fear extinction learning and to facilitate the inadequate protection against return-of-fear phenomena.

Publication Title

Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction.

Alternate Accession IDs

E-GEOD-76103

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE76108
HDAC inhibition, dopamine and long-term fear inhibition [amygdala data set]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Extinction-based exposure therapy is used in treating anxiety- and trauma-related disorders, however there is the need to improve its limited efficacy in individuals with impaired fear extinction learning and to facilitate the inadequate protection against return-of-fear phenomena.

Publication Title

Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction.

Alternate Accession IDs

E-GEOD-76108

Sample Metadata Fields

Sex, Specimen part

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)

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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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