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accession-icon GSE51912
Whole transcriptome analysis of laser capture microdissected tissues reveals site-specific programming of the host epithelial transcriptome by the gut microbiota
  • organism-icon Mus musculus
  • sample-icon 99 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Site-specific programming of the host epithelial transcriptome by the gut microbiota.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE26101
Histone acetylation and DNA demethylation of T-cells result in an anaplastic large cell lymphoma-like phenotype.
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A characteristic feature of anaplastic large cell lymphoma (ALCL) is the significant reduction of the T-cell expression program despite its T-cell origin, a finding very similar to the loss of B-cell identity of classical Hodgkin lymphoma (cHL). Previously we demonstrated that epigenetic mechanisms are active in cHL to induce this peculiar phenotype. The results show that combined DNA demethylation and histone acetylation of T-cell lines induce an almost complete extinction of the T-cell phenotype, including the down-regulation of essential T-cell receptor signalling pathway genes such as CD3, LCK and ZAP70, as well as an up-regulation of ALCL-characteristic genes. In contrast, combined DNA demethylation and histone acetylation of ALCL cells is not able to reconstitute their T-cell phenotype. This clearly demonstrates that similar epigenetic mechanisms are active in ALCL and cHL which are responsible for the extinction of their cell type characteristic phenotype.

Publication Title

Histone acetylation and DNA demethylation of T cells result in an anaplastic large cell lymphoma-like phenotype.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE44244
PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms.

Publication Title

PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE21254
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE21252
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of A/T-treated vs. untreated B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE21251
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of Hodgkin vs. B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE28079
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation: expression of PCM vs. B-cell lines
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background

Publication Title

Classical Hodgkin's lymphoma shows epigenetic features of abortive plasma cell differentiation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE30726
Deep sequencing of MYC DNA-binding sites in Burkitt's lymphoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background: MYC is a transcription factor encoded by the c-MYC gene (thereafter termed MYC). MYC is key transcription factor involved in many central cellular processes including ribosomal biogenesis. MYC is overexpressed in the majority of human tumours including aggressive B-cell lymphoma especially Burkitt's lymphoma. Although Burkitt's lymphoma is a highlight example for MYC overexpression due to a chromosomal translocation, no global analysis of MYC binding sites by chromatin immunoprecipitation (ChIP) followed by global next generation sequencing (ChIP-Seq) has been conducted so far in Burkitt's lymphoma.

Publication Title

Deep sequencing of MYC DNA-binding sites in Burkitt lymphoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE43658
Transcriptional co-factor TBLR1 controls lipid mobilization in white adipose tissue
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Lipid mobilization (lipolysis) in white adipose tissue (WAT) critically controls lipid turnover and adiposity in humans. While the acute regulation of lipolysis has been studied in detail, the transcriptional determinants of WAT lipolytic activity remain still largely unexplored. Here we show that the genetic inactivation of transcriptional co-factor transducin beta-like-related (TBLR) 1 blunts the lipolytic response of white adipocytes through the impairment of cAMP-dependent signal transduction. Indeed, mice lacking TBLR1 in adipocytes are defective in fasting-induced lipid mobilization and when placed on a high fat diet show aggravated adiposity, glucose intolerance and insulin resistance. TBLR1 levels are found to increase under lipolytic conditions in WAT of both human patients and mice, correlating with serum free fatty acids (FFA). As a critical regulator of WAT cAMP signaling and lipid mobilization, proper activity of TBLR1 in adipocytes may thus represent a critical molecular checkpoint for the prevention of metabolic dysfunction in subjects with obesity-related disorders.

Publication Title

Transcriptional cofactor TBLR1 controls lipid mobilization in white adipose tissue.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP046732
RNA-Seq analysis of mouse small intestine enteroendocrine cells
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We generated knock-in mice expressing GFP under the control of the endogenous GIP (Glucose-dependent Insulinotropic Polypeptide) promoter that enable the isolation of a purified population of small intestine K cells. Using RNA-Seq, we comprehensively characterized the transcriptomes of GIP-GFP cells as well as the entire enteroendocrine lineage derived from Neurogenin3 (Ngn3)-expressing progenitors. Overall design: We interrogated the whole transcriptome of FACS-isolated small intestine GIPGFP cells using high-throughput mRNA sequencing. We also obtained the global gene expression patterns of the entire enteroendocrine cell lineage as well as the non-enteroendocrine cell population, comprising enterocytes, goblet cells and Paneth cells. To achieve this, small intestine epithelial cells from male mice resulting from the breeding of Neurogenin3 (Ngn3)-Cre mice with ROSA26-LoxP-STOP-LoxP-tomato indicator mice were isolated based on Tomato fluorescence and negative staining for CD45. Due to the small cell numbers, we constructed each of the three RNA-Seq libraries (GIPGFP, Ngn3TOMATO, and Ngn3-) using a pool of equal amounts of individual RNA samples without RNA amplification.

Publication Title

RNA-Seq analysis of enteroendocrine cells reveals a role for FABP5 in the control of GIP secretion.

Sample Metadata Fields

No sample metadata fields

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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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