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accession-icon GSE11466
Integrin alpha6-beta4 control the expression of genes associated with cell motility, invasion and metastasis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The objective of this study was to determine the gene expression changes mediated by the alpha6beta4 integrin using MDA-MB-435 breast carcinoma cell line under normal culturing conditions (10% FCS in DMEM).

Publication Title

Integrin alpha6beta4 controls the expression of genes associated with cell motility, invasion, and metastasis, including S100A4/metastasin.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6958
FOG-1-independent transcripition by GATA-1(V205G) in G1E cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Identification of genes regulated by GATA-1 independent of the cofactor FOG-1.

Publication Title

Friend of GATA-1-independent transcriptional repression: a novel mode of GATA-1 function.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065286
GATA-1 and heme regulate the erythroid cell transcriptome.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Alas2 gene encodes the rate-limiting enzyme in heme biosynthesis. CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and the GATA-1-dependent genetic network. We discovered a GATA factor- and heme-dependent circuit that establishes the erythroid cell transcriptome. Overall design: G1E-ER-GATA-1 WT and double mutant cells were examined. Untreated WT, beta-estradiol-treated WT, beta-estradiol-treated double-mutant, and beta-estradiol/5-ALA-treated double-mutant cells were subjected to RNA-seq.

Publication Title

Mechanism governing heme synthesis reveals a GATA factor/heme circuit that controls differentiation.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP008280
Integration of Hi-C and ChIP-seq data reveals distinct types of chromatin hubs
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We have analyzed publicly available K562 Hi-C data, which enables genome-wide unbiased capturing of chromatin interactions, using a Mixture Poisson Regression Model to define a highly specific set of interacting genomic regions. We integrated multiple ENCODE Consortium resources with the Hi-C data, using DNase-seq data and ChIP-seq data for 46 transcription factors and 8 histone modifications. We classified 12 different sets (clusters) of interacting loci that can be distinguished by their chromatin modifications and which can be categorized into three types of chromatin hubs. The different clusters of loci display very different relationships with transcription factor binding sites. As expected, many of the transcription factors show binding patterns specific to clusters composed of interacting loci that encompass promoters or enhancers. However, cluster 6, which is distinguished by marks of open chromatin but not by marks of active enhancers or promoters, was not bound by most transcription factors but was highly enriched for 3 transcription factors (GATA1, GATA2, and c-Jun) and 3 chromatin modifiers (BRG1, INI1, and SIRT6). To validate the identification of the clusters and to dissect the impact of chromatin organization on gene regulation, we performed RNA-seq analyses before and after knockdown of GATA1 or GATA2. We found that knockdown of the GATA factors greatly alters the expression of genes within cluster 6. Our work, in combination with previous studies linking regulation by GATA factors with c-Jun and BRG1, provide genome-wide evidence that Hi-C data identifies sets of biologically relevant interacting loci. Overall design: RNA-seq of control, siGATA1 and siGATA2 K562 cells

Publication Title

Integration of Hi-C and ChIP-seq data reveals distinct types of chromatin linkages.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE18829
Discovering Hematopoietic Mechanisms Through Genome-Wide Analysis of GATA Factor Chromatin Occupancy
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

GATA factors interact with simple DNA motifs (WGATAR) to regulate critical processes, including hematopoiesis, but very few WGATAR motifs are occupied in genomes. Given the rudimentary knowledge of mechanisms underlying this restriction, and how GATA factors establish genetic networks, we used ChIP-seq to define GATA-1 and GATA-2 occupancy genome-wide in erythroid cells. Coupled with genetic complementation analysis and transcriptional profiling, these studies revealed a rich collection of targets containing a characteristic binding motif of greater complexity than WGATAR. GATA factors occupied loci encoding multiple components of the Scl/TAL1 complex, a master regulator of hematopoiesis and leukemogenic target. Mechanistic analyses provided evidence for cross-regulatory and autoregulatory interactions among components of this complex, including GATA-2 induction of the hematopoietic corepressor ETO-2 and an ETO-2 negative autoregulatory loop. These results establish fundamental principles underlying GATA factor mechanisms in chromatin and illustrate a complex network of considerable importance for the control of hematopoiesis.

Publication Title

Discovering hematopoietic mechanisms through genome-wide analysis of GATA factor chromatin occupancy.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE18870
Analysis of global gene expression in uninduced and -estradiol treated G1E-ER-GATA cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

Total RNA was analyzed from either uninduced or -estradiol treated G1E-ER-GATA cells to determine changes in gene expression upon induction of erythroid maturation (treated).

Publication Title

Discovering hematopoietic mechanisms through genome-wide analysis of GATA factor chromatin occupancy.

Sample Metadata Fields

Specimen part

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accession-icon GSE6835
A study of the differentiation of Murine ES cells [Scl+/hCD4 ES cells (Chung et al., 2002)] into hemangioblasts
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Molecular mechanisms that regulate the generation of hematopoietic and endothelial cells from mesoderm are poorly understood.

Publication Title

GATA2 functions at multiple steps in hemangioblast development and differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35385
GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE35384
Transcriptome analysis of differentiating normal and leukemic erythroid progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We compared the transcriptomes of differentiating cultures of ES cell derived erythroid progentor cells (ES-EP) and murine erythroleukemia (MEL) cells stably transfected with GATA-1 fused to ER.

Publication Title

A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP059378
Gene expression in wild-type vs. G2 -77 enhancer knockout myeloid progenitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

-77-/- mice exhibited late embryonic lethality, anemia, and a constellation of phenotypes. -77 conferred a unique genetic network in myeloid progenitors, endowing progenitors with potential to produce diverse progeny. Overall design: E13.5 WT or -77-/- fetal liver cells were isolated and sorted for common myeloid progenitors (CMPs) defined by Lin-Sca- CD34+FcRlow, and subjected to RNA-sequencing

Publication Title

Cis-regulatory mechanisms governing stem and progenitor cell transitions.

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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