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accession-icon GSE31365
Small-molecule inhibitor JQ1 effect on multiple myeloma cell lines
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Pathologic activation of c-Myc plays a central role in pathogenesis of several neoplasias, including multiple myeloma. However, therapeutic targeting of c-Myc has remained elusive due to its lack of a clear ligand-binding domain. We therefore targeted c-Myc transcriptional function by another means, namely the disruption of chromatin-dependent signal transduction. Members of the bromodomain and extra-terminal (BET) subfamily of human bromodomain proteins (BRD2, BRD3 and BRD4) associate with acetylated chromatin and facilitate transcriptional activation by increasing the effective molarity of recruited transcriptional activators. Notably, BRD4 marks select M/G1 genes in mitotic chromatin for transcriptional memory and direct post-mitotic transcription, via direct interaction with the positive transcription elongation factor complex b (P-TEFb). Because c-Myc is known to regulate promoter-proximal pause release of Pol II, also through the recruitment of P-TEFb, we evaluated the selective small-molecule inhibitor of BET bromodomains, JQ1, as a chemical probe to interrogate the role of BET bromodomains in Myc-dependent transcription and to explore their role as therapeutic targets in c-Myc-driven neoplasias.

Publication Title

BET bromodomain inhibition as a therapeutic strategy to target c-Myc.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP109011
Multipotent Peripheral Glial Cells Generate Neuroendocrine Cells of the Adrenal Medulla
  • organism-icon Mus musculus
  • sample-icon 768 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Cells producing adrenalin are largely derived from nerve-associated Schwann cell precursors via an intermediate progenitor “bridge” cell. We demonstrate that large numbers of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs) Overall design: SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland where they detach from the nerve and form post-synaptic neuroendocrine chromaffin cells. An intricate molecular logic drives two sequential phases of gene expression, one unique for a distinct transient cellular state and another for cell-type specification. Subsequently, these programs downregulate SCP- and upregulate chromaffin-cell-gene networks. The adrenal medulla forms through limited cell expansion and requires the recruitment of numerous SCPs. Thus, peripheral nerves serve as a stem cell niche for neuroendocrine system development.

Publication Title

RNA velocity of single cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP150534
Metabolic labeling of Hek293 cells using 4-thiouracil
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Hek293 cells were metabolically labelled using 4-thiouracil as described in (Schwalb et al, Science. 2016 Jun 3;352(6290):1225-8) but without fragmentation, and then bulk RNA was prepared for sequencing using the STRT method (Islam et al, Genome Res. 2011 Jul;21(7):1160-7). Samples were incubated in duplicate for 5, 15 and 30 minutes and included an unlabeled control representing the steady-state expression state. Overall design: 2 samples each of 4 incubation times, 2 cDNA preparations, 2 tagmentation replicates, and 2 biological replicates

Publication Title

RNA velocity of single cells.

Sample Metadata Fields

Cell line, Subject

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accession-icon E-MEXP-268
Transcription profiling of asymptomatic and symptomatic atherosclerotic plaques from the same patient
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.

Publication Title

Microarray analysis reveals overexpression of CD163 and HO-1 in symptomatic carotid plaques.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Subject, Time

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accession-icon GSE51350
Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1

Publication Title

Ikaros is absolutely required for pre-B cell differentiation by attenuating IL-7 signals.

Sample Metadata Fields

Specimen part

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accession-icon GSE75712
WT and Ikaros-deficient follicular B cells stimulated with anti-IgM
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We have observed that follicular B cells from mice with a hypomorphic mutation (IkL/L) in the Ikzf1 gene (which encodes the Ikaros transcription factor) exhibit an increased proliferative response to anti-IgM stimulation (Kirstetter et al, Eur J Immunol, 32:720-30, 2002). We asked if Ikaros controls the transcriptional response that unfolds after activation, or if differences in the transcriptional landscape of resting B cells could explain the altered response. To this end, we have determined the transcriptome of unstimulated WT and IkL/L follicular B cells, as well as that of cells stimulated for 3h and 12h with anti-IgM. Samples from 2 independent experients were analyzed.

Publication Title

Ikaros limits follicular B cell activation by regulating B cell receptor signaling pathways.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE84813
Exon level expression profile of MCF7 cells with p53 splice variant knocked out 4hr post 20gy irradiation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

In order to explore the funciton of p53 splice variant in DNA damage response, we utilized CRISPR-cas9 genome editing technique to specifically knock out this variant in MCF7 cells.

Publication Title

Identification of a DNA Damage-Induced Alternative Splicing Pathway That Regulates p53 and Cellular Senescence Markers.

Sample Metadata Fields

Treatment

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accession-icon GSE114108
Expression data from mouse monocyte- and common- dendritic progenitors (MDP and CDP) from Ikaros mutant in response to gamma-secretase inhibitor (GSI)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Ikaros hypomorphic mice (IkL/L) show plasmacytoid dendritic cell (pDC) defects with an absence of pDCs in the peripheral organs and a reduction of pDCs in the bone marrow (BM). Moreover in vitro differentiation of pDC from IkL/L total BM cells is also defective.

Publication Title

Ikaros cooperates with Notch activation and antagonizes TGFβ signaling to promote pDC development.

Sample Metadata Fields

Treatment

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accession-icon GSE48203
Expression data from tumoral thymocytes and DP thymocytes expressing an activated form of b-catenin in mouse T cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To assess the importance of the Wnt pathway during T cell develoment, we generated a mouse line (R26-cat) in which high levels of active -catenin are maintained throughout T cell development. Young R26-cat mice (6-week-old) show a differentiation block at the CD4+CD8+ DP stage. All R26-cat mice develop T cell leukemias with a DP phenotype at 5-6 months of age.

Publication Title

β-Catenin activation synergizes with Pten loss and Myc overexpression in Notch-independent T-ALL.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP059237
Chromosomal deletions linked to p53 loss of heterozygosity promote cancer through p53-independent mechanisms
  • organism-icon Mus musculus
  • sample-icon 95 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The purpose of current study is to identify the differentiated gene expression associated with mouse 11B3 deletion, syntenic to human chromosome 17p13.1. We compared four different mouse acute myeloid leukemia cells, freshly isolated from mouse bone marrows with either 11B3fl/p53fl;shNf1;shMll3;Vav1-Cre or p53fl/fl;shNf1;shMll3;Vav1-Cre. The RNA-seq results indicate that genes located on chromosome 11B3 mostly reduce gene expression level in 11B3 deleted leukemia cells. Overall design: Examination RNA expression level in 11B3-deleted vs p53-loss only samples.

Publication Title

Deletions linked to TP53 loss drive cancer through p53-independent mechanisms.

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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