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accession-icon GSE26994
PU.1 and C/EBPalpha synergistically program distinct response to NF-kappaB activation through establishing monocyte-specific enhancers
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PU.1 and C/EBP(alpha) synergistically program distinct response to NF-kappaB activation through establishing monocyte specific enhancers.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE26868
PU.1 and C/EBPalpha synergistically program distinct response to NF-kappaB activation through establishing monocyte specific enhancers (expression data)
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Unraveling the complexity of transcriptional programs coded by different cell types has been one of the central goals of cell biology. Using genome-wide location analysis, we examined how two different cell types generate different responses to the NF-kappaB signaling pathway. We showed that, after tumor necrosis factor-alpha (TNF-alpha) treatment, NF-kappaB p65 subunit binds to distinct genome locations and subsequently induces different subsets of genes in human monocytic THP-1 cells versus HeLa cells . Interestingly, the differential p65 binding in two cell types correlates with pre-existing cell-type specific enhancers prior to TNF-alpha stimulation, marked by histone modifications. We also found that two transcription factors, PU.1 and C/EBPalpha, appear to synergistically mediate enhancer creation and affect NF-kappaB target selection in THP-1 cells. In HeLa cells, co-expression of PU.1 and C/EBPalpha conferred TNF-alpha responsiveness to a subset of THP-1 specific NF-kappaB target genes. These results suggest that the diversity of transcriptional programs in mammalian cells arises, at least in part, from pre-existing enhancers that are established by cell specific transcription factors.

Publication Title

PU.1 and C/EBP(alpha) synergistically program distinct response to NF-kappaB activation through establishing monocyte specific enhancers.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE36403
Profiles of Epigenetic Histone Post-translational Modifications at Type 1 Diabetes Susceptible Genes
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Profiles of epigenetic histone post-translational modifications at type 1 diabetes susceptible genes.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon GSE36084
Gene expression data from human lymphocytes
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. We used the chromatin-immunoprecipitation-linked-to-microarray approach to profile key histone PTMs, including H3-lysine-4 trimethylation (H3K4me3), H3K27me3, H3K9me3, H3K9 acetylation (H3K9Ac) and H4K16Ac at genes within the T1D susceptible loci in lymphocytes, and H3K4me3, H3K9me2, H3K9Ac and H4K16Ac at the IDDM1 region in monocytes of T1D patients and healthy controls separately. We screened for potential variations in histone PTMs using computational methods to compare datasets from T1D and controls. Interestingly, we observed marked variations in H3K9Ac levels at the upstream regions of HLA-DRB1 and HLA-DQB1 within the IDDM1 locus in T1D monocytes relative to controls. Additional experiments with THP-1 monocytes demonstrated increased expression of HLA-DRB1 and HLA-DQB1 in response to interferon- and TNF-treatment that were accompanied by changes in H3K9Ac at the same promoter regions as that seen in the patient monocytes. These results suggest that the H3K9Ac status of HLA-DRB1 and HLA-DQB1, two genes highly associated with T1D, may be relevant to their regulation and transcriptional response towards external stimuli. Thus, the promoter/enhancer architecture and chromatin status of key susceptible loci could be important determinants in their functional association to T1D susceptibility.

Publication Title

Profiles of epigenetic histone post-translational modifications at type 1 diabetes susceptible genes.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon SRP018312
RNA-Sequencing Analysis of High Glucose Treated Monocytes Reveals Novel Transcriptome Signatures and associated Epigenetic Profiles
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We report high throughput transcriptomic profiling with RNA-Sequencing (RNA-Seq) to uncover network responses in human THP-1 monocytes treated with high glucose (HG). Overall design: Examination of differential expression between normal and high glucose condition in THP1 cells.

Publication Title

RNA-sequencing analysis of high glucose-treated monocytes reveals novel transcriptome signatures and associated epigenetic profiles.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP154186
Single cell RNA sequencing of primary-isolated erythroid progenitors [Days 1-3]
  • organism-icon Mus musculus
  • sample-icon 576 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

single cell RNA sequencing of freshly isolated mouse BFU-E (burst forming unit-erythroid ) cells cultured for 1, 2, or 3 days with and without 100nM dexamethasone Overall design: six 96 well plates

Publication Title

Rate of Progression through a Continuum of Transit-Amplifying Progenitor Cell States Regulates Blood Cell Production.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP154147
Single cell RNA sequencing of primary-isolated erythroid progenitors [BFUE, CFUE, intermediates]
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Single cell RNA sequencing of freshly isolated mouse burst forming unit-erythroid (BFU-E) , colony forming unit-erythroid (CFU-E), and intermediate stages of erythroid development cells. Overall design: One 96 well plate with 24 BFU-E, 24 CFU-E, 24 cells with 25-35% expression of CD71/CD24, and 24 cells with 50-60% expression of CD71/CD24.

Publication Title

Rate of Progression through a Continuum of Transit-Amplifying Progenitor Cell States Regulates Blood Cell Production.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP154149
Single cell RNA sequencing of primary-isolated erythroid progenitors [daughter cells]
  • organism-icon Mus musculus
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Single cell mouse BFU-E (burst forming unit-erythroid ) were FACS-deposited into individual wells of a 96-well plate containing PCM either with or without 100 nM dexamethasone. After 16hrs cells from wells that contained a single pair of daughter cells were separated and each individual daughter cell transcriptome was obtained by single cell RNA-seq. Overall design: 13 daughter cells pairs untreated and 13 pairs treated with 100 nM dexamethasone.

Publication Title

Rate of Progression through a Continuum of Transit-Amplifying Progenitor Cell States Regulates Blood Cell Production.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon SRP187073
Single cell RNA sequencing of primary-isolated erythroid progenitors [BFUEs_Set2]
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Single cell RNA sequencing of freshly isolated mouse burst forming unit-erythroid (BFU-E). Overall design: One 96 well plate with 24 BFU-E.

Publication Title

Rate of Progression through a Continuum of Transit-Amplifying Progenitor Cell States Regulates Blood Cell Production.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP048892
Mus musculus Transcriptome or Gene expression
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Tmem67 knock-out mouse model of Meckel-Gruber syndrome type 3 (MKS3, MIM #607361) and Joubert syndrome type (JBTS6, #610688): investigation into differential gene expression in the early post-natal (P0) cerebullum

Publication Title

Variable expressivity of ciliopathy neurological phenotypes that encompass Meckel-Gruber syndrome and Joubert syndrome is caused by complex de-regulated ciliogenesis, Shh and Wnt signalling defects.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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