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accession-icon GSE113503
Gene expression data from E14.5 Pogz-WT and Pogz-KO fetal livers.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Fetal and adult -globin gene expression is tightly regulated during human development. Fetal globin genes are transcriptionally silenced during embryogenesis through the process of hemoglobin switching. Efforts to understand the transcriptional mechanism(s) behind fetal globin silencing have led to novel strategies to derepress fetal globin expression in the adult, which could alleviate symptoms in hereditary b-globin disorders including sickle cell disease (SCD) and -thalassemia. We identified a novel zinc finger protein, pogo transposable element with zinc finger domain (Pogz), expressed in mouse and human hematopoietic stem and progenitor cells, which represses embryonic b-like globin gene expression in mice. Ablation of Pogz expression in adult hematopoietic cells in vivo results in persistence of embryonic b-like globin expression without significantly affecting erythroid development or mouse survival. Elevated embryonic -like globin expression correlates with reduced expression of Bcl11a, a known repressor of embryonic -like globin expression, in Pogz-/- fetal liver cells. Pogz binds to the Bcl11a promoter, and, to erythroid specific intragenic regulatory regions. Importantly, Pogz+/- mice develop normally, but show elevated embryonic b-like globin expression in peripheral blood cells, demonstrating that reducing Pogz levels results in persistence of embryonic b-like globin expression. Finally, knockdown of POGZ in primary human CD34+ hematopoietic stem and progenitor cell derived erythroblasts, reduces BCL11A expression and increases fetal hemoglobin expression. These findings are significant since new therapeutic targets and strategies are needed to treat the increasing global burden of b-globin disorders.

Publication Title

POGZ Is Required for Silencing Mouse Embryonic β-like Hemoglobin and Human Fetal Hemoglobin Expression.

Sample Metadata Fields

Specimen part

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accession-icon GSE71062
Gene expression analysis of BE(2)C cells treated with SSRP1 and MYCN siRNAs
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

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accession-icon GSE71059
Gene expression analysis of BE(2)C cells treated with SSRP1 siRNA
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconAgilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Amplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma

Publication Title

Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE71060
Gene expression analysis of BE(2)C cells treated with MYCN siRNA (MYCN1 #SI03087518)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Amplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma

Publication Title

Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE8431
Microarray screening of RARgamma responsive genes in F9 teratocarcinoma cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We compared the differentially expressed genes between the F9 Wt cells and F9 RAR gamma knock out cells before and after RA treatment. 3 replicates for each conditions.

Publication Title

Gene expression profiling elucidates a specific role for RARgamma in the retinoic acid-induced differentiation of F9 teratocarcinoma stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7528
Gene expression of Wt vs CYP26A1-/- murine ES cells treated with control or 100 nM RA for 8 or 72 hr.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goal of this study was to identify genes that are differentially expressed after genetic deletion of both alleles of the Cyp26a1 gene in murine embryonic stem cells. Cyp26a1 codes for the CYP26A1 enzyme which metabolizes RA to polar RA metabolites, such as 4-oxo-RA and 4-OH-RA. CYP26A1-/- ES cells do not metabolize RA within 48 hours of RA treatment while in Wt ES cells, polar RA metabolites are already detectable by 8 hr. In addition, the absence of CYP26A1 enzyme increases intracellular RA levels. By gene microarray analysis, we wanted to identify genes that would be affected by the lack of the Cyp26a1 gene.

Publication Title

CYP26A1 knockout embryonic stem cells exhibit reduced differentiation and growth arrest in response to retinoic acid.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP031478
Altered Epigenetic Regulation of Homeobox Genes in Human Oral Squamous Cell Carcinoma Cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

To gain insight into the molecular changes during OSCC carcinogenesis, we performed unbiased, whole genome deep sequencing (RNA-seq) using RNA isolated from cultured, human TERT-immortalized, non-tumorigenic OKF6-TERT1R and OSCC SCC-9 cells. Overall design: OKF6-TERT1R cells and SCC-9 cells were plated in 10 cm2 tissue culture plates at the density of 2 × 106 cells/plate and treated with 1 µM RA or vehicle (0.1% ethanol) for 48 hours. Experiment includes 3 independent biological replicates.

Publication Title

Altered histone mark deposition and DNA methylation at homeobox genes in human oral squamous cell carcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31280
Transcript level in F9 teratocarcinoma WT and RARalpha knockout in presence and absence of all-trans retinoic acid
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Retinoic acid receptors (RARs) , and are key regulators of embryonic development. Hematopoietic differentiation is regulated by RAR, and several types of leukemia show aberrant RAR activity. We demonstrate that RAR plays an important role in cellular memory and imprinting by regulating the CpG methylation status of specific promoter regions.

Publication Title

Epigenetic regulation by RARα maintains ligand-independent transcriptional activity.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP019757
mRNA profiling of GGT-HIF2aM3 (gamma-HIF2alphaM3) kidney cortex
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The complete transcriptomes of kidney cortex from 3 ?-HIF2aM3 18 month old TG+ male mice and 3 age matched wild type (WT) C57BL/6 male mice were sequenced on an Illumina HiSeq2000 Sequencer. Overall design: Examination of complete transcriptome of kidney cortex between ?-HIF2aM3 TG+ male mice and wild type C57BL/6 male mice

Publication Title

Activation of HIF2α in kidney proximal tubule cells causes abnormal glycogen deposition but not tumorigenesis.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE9978
Genes plus and minus LIF
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This study was undertaken in order to characterize the functions of Rex-1 and identify potential Rex-1 target genes.Both alleles of the Rex-1 gene were disrupted in J1 mouse embryonic stem cells. Gene expression levels in one of the resulting Rex-1 knockout cell lines was compared to that of J1 wild type cells.

Publication Title

Analysis of Rex1 (zfp42) function in embryonic stem cell differentiation.

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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