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accession-icon GSE49886
KDM6 Inhibition induces DNA Damage Response (DDR) during ESC Differentiation but not during self-renewal.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The discovery of the first histone demethylase in 2004 (LSD1/KDM1) opened new avenues for the understanding of how histone methylation impacts cellular functions. A great number of histone demethylases have been identified since, which are potentially linked to gene regulation as well as to stem cell self-renewal and differentiation. KDM6A/UTY and KDM6B/JMJD3 are both H3K27me3/2-specific histone demethylases, which are known to play a central role in regulation of posterior development, by regulating HOX gene expression. So far nothing is known about the role of histone lysine demethylases (KDMs) during early hematopoiesis. We are studying the role of KDM6A and KDM6B on self-renewal, global gene expression and on local and global chromatin states in embryonic stem cells (ESCs) and during differentiation. In order to completely abrogate KDM6 demethylase activity in ESCs we employed a specific inhibitor (GSK-J4, Kruidenier et al. 2012). Treatment of ESCs with GSK-J4 had no effect on viability and proliferation . However, ESC differentiation in the presence of GSK-J4 was completely abrogated. In conclusion we show that ESC differentiation is completely blockend in the absence of any H3K27 demethylase activity.

Publication Title

Inhibition of KDM6 activity during murine ESC differentiation induces DNA damage.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP144076
Nascent RNA Sequencing after NMYC activation in SH-EP MYCNER cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

In order to distinguish transcription changes from RNA modification and post transcription changed, nascent RNA seq via metabolic labeling of freshly synthesized RNA was carried out using 4sU labeling/biotin purification. Overall design: nascent RNA was extractred post N-MYC activation and compared with untreated cells nascent RNA to gather fold changes of pre-mRNA on gene basis.

Publication Title

MYC Recruits SPT5 to RNA Polymerase II to Promote Processive Transcription Elongation.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP059337
Gene expression profiling of six MEF cell genotypes (wild type, ß2SP+/-, ß2SP-/-, SMAD3+/-, SMAD3-/-, and ß2SP+/-; SMAD3+/-)
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene expression profiling was carried out in six (wild type, ß2SP+/-, ß2SP-/-, SMAD3+/-, SMAD3-/- and ß2SP+/-/ SMAD3+/-) different mouse knockout embryonic fibroblast (MEF) cells. Beta-2-spectrin (ß2SP) is a dynamic intracellular non-pleckstrin homology (PH)-domain protein that belongs to a family of polypeptides that have been implicated in conferring cell polarity. Spectrins have been linked to multiple signaling pathways, including cell cycle regulation, DNA repair and TGFß signaling. In this study, we report a major role of the TGFß/Smad3 adaptor ß2-Spectrin in conserving genomic integrity from alcohol-induced DNA damage and describe a novel pathway that protects genomes from genotoxic stresses. To determine the mechanism for the oncogenic switch, and whether it is related to the role of ß2SP in TGF-ß signaling transduction or secondary to its cytoskeletal functions, we analyzed disruption of two elements of the TGF-ß pathway by generating double heterozygous Sptbn1+/-/Smad3+/- mice. Overall design: Whole-transcriptome RNA sequencing MEF cells of the following genotypes was carried out on an Illumina HiSeq 2000 sequencer: wildtype, heterozygous Beta-2-spectrin knockout (ß2SP+/-), homozygous Beta-2-spectrin knockout (ß2SP-/-), heterozygous SMAD3 (Mothers against decapentaplegic, Drosophila, Homolog of 3, SMAD3+/-), homozygous knockout SMAD3-/-, and double heterozygous mutation of Beta-2-spectrin and SMAD3 (ß2SP+/-/ SMAD3+/-).

Publication Title

TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP059331
Gene expression analysis of mice liver tumors isolated from ß2SP+/-; SMAD3+/- mice
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene expression profiling was carried out in two liver tumors and one normal liver isolated from ß2SP+/-; SMAD3+/- mice, and one normal liver isolated from wild type mouse. Whole-transcriptome sequencing of these 4 liver tissues. Overall design: Whole-transcriptome RNA sequencing of the 4 different samples

Publication Title

TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP059324
Gene expression analysis of human cell lines established from normal patient''s fibroblast and BWS patients with known mutations in the CDKN1C and KCNQ1OT1
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Gene expression profiling was carried out in one normal human fibroblast cell line established from normal people and three different cell lines established from BWS patients to characterize the molecular mechanisms relevant to the etiology of BWS and tumor development. Whole-transcriptome sequencing of three BWS fibroblastic cell lines was established from patients with mutation in the CDKN1C mutation (CDKN1C+ cell line), and loss of methylation in the KCNQ1OT1 region (KvDMR+ cell line: with KvDMR molecular defect, and KvDMR- cell line: absence of KvDMR molecular defect but it had some clinical signs of BWS) Overall design: Whole-transcriptome RNA sequencing of the 4 different cell lines

Publication Title

TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP055098
Gene expression analysis of wild-type and Beta-2-spectrin homozygous knockout (ß2SP-/-) mouse embryonic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene expression profiling was carried out in wild and ß2SP-/- (Sptbn1 -/-) mouse embryonic fibroblast (MEF) cells. Beta-2-spectrin (ß2SP) is a dynamic intracellular non-pleckstrin homology (PH)-domain protein that belongs to a family of polypeptides that have been implicated in conferring cell polarity. Spectrins have been linked to multiple signaling pathways, including cell cycle regulation, DNA repair and TGFß signaling. In this study, we report a major role of the TGFß/Smad3 adaptor ß2-Spectrin in conserving genomic integrity from alcohol-induced DNA damage and describe a novel pathway that protects genomes from genotoxic stresses. Overall design: Whole-transcriptome RNA sequencing of wild-type and ß2SP knockout (ß2SP-/-) mouse embryonic fibroblasts was carried out on an Illumina HiSeq 2000 sequencer. The raw data quality was assessed using a FastQC software. Adaptor presence was tested using Trimmomatic. The readings were then aligned to the NCBI mouse reference genome build 37.2 using the splice-aware aligner Tophat2 v2.0.10. Transcript quantification, normalization and assembly were carried out with Cufflinks. A gene model gtf file corresponding to the NCBI mouse reference genome build 37.2 was used in the quantification. Cuffdiff2, part of the Cufflinks suite of tools, was used to identify significant differences in gene expression profiles between the wild-type and ß2SP-/- MEF cells.

Publication Title

TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33981
Microarray analysis of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposed Amputated Adult Zebrafish Heart Ventricles
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

The purpose of this experiment is to understand which transcripts are differentially expressed following exposure to TCDD.

Publication Title

TCDD inhibits heart regeneration in adult zebrafish.

Sample Metadata Fields

Treatment

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accession-icon SRP169618
Transcriptomic analysis of different human cardiac cell types produced in vitro from human pluripotent stem cells or derived from patients.
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The epicardium, an epithelium covering the heart, is essential for cardiac development. During embryogenesis, the epicardium provides instructive signals for the growth and maturation of cardiomyocytes and for coronary angiogenesis. We generated an in vitro model of human embryonic epicardium derived from human pluripotent stem cells (hPSC-epi). These cells were able to differentiate into cardiac fibroblasts (cf) and smooth muscle cells (smc) in vitro (hPSC-epi-cf and hPSC-epi-smc respectively). Furthermore, we showed that they improved maturation of hPSC-derived cardiomyocytes (hPSC-cardio) in vitro while neural crest cells derived from hPSC (hPSC-NC) could not. Furthermore, they improved survival of hPSC-cardio and stimulated angiogenesis when injected in a rat model of myocardium infarction. We performed mRNA sequencing of the hPSC-epi, hPSC-epi-cf, hPSC-smc and hPSC-NC in order to identify the secreted molecules specifically produced by the hPSC-epi and/or its derivatives in comparison with the hPSC-NC. Vascular smooth muscle cells have different embryonic origins and different properties depending on their location in the body. The coronary smooth muscle cells come from the epicardium while the aortic ones come from the mesoderm or the neural crest. We performed mRNA sequencing of human coronary artery smc and human aortic smc to identify a specific signature of the coronary smc. We also compared the genes expressed in the hPSC-epi-smc and the smc derived from hPSC-derived lateral plate mesoderm. Overall design: For hPSC-derived samples the three replicates are coming from three different in vitro differentiations from H9. For the human primary cells, the triplicates are technical replicates (three different wells from the same culture at the same passage)

Publication Title

Epicardial cells derived from human embryonic stem cells augment cardiomyocyte-driven heart regeneration.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE8608
MDM from COPD patients and healthy subjects after treatment with LPS or fine and ultrafine particles
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study gene expression of monocyte-derived macrophages (MDM) from chronic obstructive pulmonary disease (COPD) patients and healthy subjects was investigated. MDM were treated with LPS, a combination of fine TiO2 and ultrafine Printex90 particles, or remained untreated.

Publication Title

Tissue-specific induction of ADAMTS2 in monocytes and macrophages by glucocorticoids.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24514
Expression data from human MSI colorectal cancer and normal colonic mucosa
  • organism-icon Homo sapiens
  • sample-icon 49 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Microsatellite instability (MSI), caused by defective mismatch repair, is observed in a subset of colorectal cancers (CRCs). We evaluated somatic mutations in microsatellite repeats of genes chosen based on reduced expression in MSI CRC and existence of a coding mononucleotide repeat.

Publication Title

Candidate driver genes in microsatellite-unstable colorectal cancer.

Sample Metadata Fields

Specimen part

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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