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accession-icon SRP020090
Pbx and Prdm1a transcription factors differentially regulate subsets of the fast skeletal muscle program in zebrafish
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The basic helix-loop-helix factor Myod initiates skeletal muscle differentiation by directly and sequentially activating sets of muscle differentiation genes, including those encoding muscle contractile proteins. We hypothesize that Pbx homeodomain proteins direct Myod to a subset of its transcriptional targets, in particular fast twitch muscle differentiation genes, thereby regulating the competence of muscle precursor cells to differentiate. We have previously shown that Pbx proteins bind with Myod on the promoter of the zebrafish fast muscle gene mylpfa and that Pbx proteins are required for Myod to activate mylpfa expression and the fast-twitch muscle-specific differentiation program in zebrafish embryos. Here we have investigated the interactions of Pbx with another muscle fiber-type regulator, Prdm1a, a SET-domain DNA-binding factor that directly represses mylpfa expression and fast muscle differentiation. The prdm1a mutant phenotype, early and increased fast muscle differentiation, is the opposite of the Pbx-null phenotype, delayed and reduced fast muscle differentiation. To determine whether Pbx and Prdm1a have opposing activities on a common set of genes, we used RNA-seq analysis to globally assess gene expression in zebrafish embryos with single- and double-losses-of-function for Pbx and Prdm1a. We find that the levels of expression of certain fast muscle genes are increased or approximately wild type in pbx2/4-MO;prdm1a-/- embryos, suggesting that Pbx activity normally counters the repressive action of Prdm1a for a subset of the fast muscle program. However, other fast muscle genes require Pbx but are not regulated by Prdm1a. Thus, our findings reveal that subsets of the fast muscle program are differentially regulated by Pbx and Prdm1a. Our findings provide an example of how Pbx homeodomain proteins act in a balance with other transcription factors to regulate subsets of a cellular differentiation program. Overall design: Total RNA samples were genotyped and pooled for 4 sample types: control-MO;prdm1+/+; control-MO;prdm1-/-; pbx2/4-MO;prdm1+/+; and pbx2/4-MO;prdm1-/- embryos at the 10 somite (s) stage from three independent sets of egg collections/injections.

Publication Title

Pbx and Prdm1a transcription factors differentially regulate subsets of the fast skeletal muscle program in zebrafish.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8428
The expression profiles of control embryos and pbx2-MO;pbx4-MO embryos at 10 somites and at 18 somites.
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Pbx homeodomain proteins have been implicated in the regulation of gene expression during muscle development. Whether Pbx proteins are required broadly for the regulation of muscle gene expression or are required for the expression of a specific subset of muscle gene expression is not known. We employed microarrays to determine the requirements for Pbx proteins during zebrafish development.

Publication Title

Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP051986
Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

MyoD and NeuroD2 are master regulators of myogenesis and neurogenesis and bind to a "shared" E-box sequence (CAGCTG) and a "private" sequence (CAGGTG or CAGATG, respectively). To determine whether private-site recognition is sufficient to confer lineage-specification, we generated a MyoD-mutant with the DNA binding specificity of NeuroD2. Our results demonstrate that redirecting MyoD binding from MyoD-private sites to NeuroD2-private sites, despite preserved binding to the MyoD/NeuroD2-shared sites, is sufficient to change MyoD from a master regulator of myogenesis to a master regulator of neurogenesis. Overall design: RNA-seq profiling of mouse P19 cells transfected with MyoD, NeuroD2 and chimera mutants. The chimeric mutants are MyoD with the bHLH domain replaced with the NeuroD2 bHLH domain.

Publication Title

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE86999
Microarray analysis of IL-17 gene transfer in murine dorsal skin.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Comparison of dorsal skin gene expression between GFP and IL-17 gene transfer in C57BL/6J mice

Publication Title

T Cell-Independent Mechanisms Associated with Neutrophil Extracellular Trap Formation and Selective Autophagy in IL-17A-Mediated Epidermal Hyperplasia.

Sample Metadata Fields

Specimen part

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accession-icon GSE99039
A blood-based gene signature characterizing Idiopathic Parkinson's disease
  • organism-icon Homo sapiens
  • sample-icon 558 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Establishing reliable biomarkers for assessing and validating clinical diagnosis at early prodromal stages of Parkinsons disease is crucial for developing therapies to slow or halt disease progression. Here, we present the largest study to date using whole blood gene expression profiling from over 500 individuals to identify an 87-gene blood-based signature. Our gene signature effectively differentiates between idiopathic PD patients and controls in both a validation cohort and an independent test cohort, and further highlights mitochondrial metabolism and ubiquitination/proteasomal degradation as potential pathways disrupted in Parkinsons disease.

Publication Title

Analysis of blood-based gene expression in idiopathic Parkinson disease.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE29672
The transcription factors Snail and Slug activate the TGF-B signaling pathway in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling to determine transcriptome changes following Snail or Slug expression in MCF-7 breast cancer cells

Publication Title

The transcription factors Snail and Slug activate the transforming growth factor-beta signaling pathway in breast cancer.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE37179
Expression data from infected with Neisseria gonorrhoeae (GC) and uninfected bone marrow derived macrophages from wild type (C67BL/6) and Nod2 knock out mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In this dataset we include the data obtained from 3 hour stimulation with Neisseria gonorrhoeae (GC) of bone marrow macrophages(BMDM) from wild type (C57BL/6) and Nod2 knock out mice (in C57BL/6 background).

Publication Title

Activation of NOD receptors by Neisseria gonorrhoeae modulates the innate immune response.

Sample Metadata Fields

Specimen part

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accession-icon GSE59485
Expression data from bovine nucleus pulposus interverteral disc cells
  • organism-icon Bos taurus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

Assessment of the putative differential gene expression profiles in high osmolality-treated bovine nucleus pulposus intervertebral disc cells for a short (5 h) and a long (24 h) time period. Identification of novel genes up- or down-regulated as an early or a late response to hyperosmotic stress.

Publication Title

Deficiency in the α1 subunit of Na+/K+-ATPase enhances the anti-proliferative effect of high osmolality in nucleus pulposus intervertebral disc cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE7238
Ets2 is required for trophoblast stem cell self renewal
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconSentrix Mouse-6 Expression BeadChip

Description

The Ets2 transcription factor is essential for the development of the mouse placenta and for generating signals for embryonic mesoderm and axis formation. Using a conditional targeted Ets2 allele, we show that Ets2 is essential for trophoblast stem (TS) cells self renewal. Inactivation of Ets2 results in slower growth, increased expression of a subset of differentiation associated genes and decreased expression of several genes implicated in TS self renewal. Among the direct TS targets of Ets2 is Cdx2, a key master regulator of TS cell state. In addition other Ets2 responsive genes include Pace4, Errb, Socs2 and Bmp4. Thus Ets2 contributes to the regulation of multiple genes important for maintaining the undifferentiated state of TS cells and as candidate signals for embryonic development.

Publication Title

Ets2 is required for trophoblast stem cell self-renewal.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8040
CD34 antigen role in haematopoietic commitment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Role of CD34 antigen in myeloid differentiation of human hematopoietic progenitor cells.

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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