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accession-icon GSE32526
Expression data from breast cancer tumor-initiating cells
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have generated tumorigenic (S2N) and non-tumorigenic (S2), normal-like to basal-like breast cancer cell lines from primary tumors. At high in vivo inoculation cell numbers of 10^6 cells/mouse both S2N and S2 monolayer as well as sphere culture cells grew at similar rates. However, at low inoculation cell numbers down to 10^3 cells only S2N sphere cells generated xenograft tumors. mRNA profiling revealed a unique cluster pattern of the tumorigenic S2N sphere cells, but a detailed analysis of TIC relevant transcription factors like Oct3, Sox and Nanog family members, Myc, Slug or Twist1 revealed no consistently increased expression in the highly tumorigenic cell lines. Our data indicate that the intrinsic genetic and functional markers investigated are not solely indicative of the in vivo tumorigenicity of putative breast tumor-initiating cells.

Publication Title

Established breast cancer stem cell markers do not correlate with in vivo tumorigenicity of tumor-initiating cells.

Sample Metadata Fields

Disease, Cell line

View Samples
accession-icon SRP067240
Integrative Single-Cell Transcriptomics Reveals Molecular Networks Defining Neuronal Maturation during Neurogenesis
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Neurogenesis in the adult hippocampus contributes to information processing critical for cognition, adaptation, learning and memory, and is implicated in numerous neurological disorders. New neurons are continuously produced from neural stem cells via a well-controlled developmental process. The immature neuron stage defined by doublecortin (DCX) expression is the most sensitive to regulation by extrinsic factors. However, little is known about the dynamic biology within this critical interval that drives maturation and confers susceptibility to regulating signals. This study aims to test the hypothesis that DCX-expressing immature neurons in adult mouse hippocampus progress through developmental stages via activity of specific transcriptional networks. Using single-cell RNA-seq combined with a novel integrative bioinformatics approach, we discovered that individual immature neuron can be classified into distinct developmental subgroups based on characteristic gene expression profiles and subgroup-specific markers. Comparisons between immature and more mature subgroups revealed novel pathways involved in neuronal maturation. Genes enriched in more immature cells shared significant overlap with genes implicated in neurodegenerative diseases, while genes positively associated with neuronal maturation were enriched for autism-related gene sets. Our study thus discovers molecular signatures of individual adult-born immature neurons and unveils potential novel targets for therapeutic approaches to treat neurodevelopmental and neurological diseases. Overall design: mRNA sequencing and expression estimation in 64 individual DCX-dsRed+ cells isolated from transgenic DCX-dsRed mice by FACS sorting

Publication Title

Integrative Single-Cell Transcriptomics Reveals Molecular Networks Defining Neuronal Maturation During Postnatal Neurogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE3356
Effects of metoprolol and nebivolol on gene expresion in human coronary smooth muscle cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Human coronary smooth muscle cells were treated with two different -blocker (metoprolol and nebivolol). RNA from three replicates of each, treated and the untreated control group, were isolated and the expression profiles were determined using Affymetrix Human Genechip U133A arrays. Comparisons between the sample groups allow the identification of genes with different expression patterns between the treated and untreated control cells.

Publication Title

Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE72240
Expression data from fetal sheep immunocytes
  • organism-icon Ovis aries
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Ovine Gene 1.1 ST Array (ovigene10st)

Description

study investigating the initiation of systemic inflammatory signaling in fetuses exposed to TLR-4 agonist lipopolysaccharides from E.coli

Publication Title

Outside-in? Acute fetal systemic inflammation in very preterm chronically catheterized sheep fetuses is not driven by cells in the fetal blood.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE15935
Expression data from 'nave' and HVC-replicon containing Huh7 cells (Clone A cells)
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cyclophilin binding drugs, NIM811 and cyclosporin A (CsA), inhibit the replication of HCV replicon.

Publication Title

Multiple cyclophilins involved in different cellular pathways mediate HCV replication.

Sample Metadata Fields

Time

View Samples
accession-icon SRP074420
RNASeq of MV4;11 cells transduced with scramble shRNA or BRD4 shRNA in combination with DMSO or SGC0946
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Central to the molecular pathogenesis of MLL leukaemia is the abnormal co-optation of members of transcription complexes including disrupter of telomeric silencing 1-like (DOT1L) and bromodomain containing protein 4 (BRD4). Consequently, targeted therapies against DOT1L and BRD4 are currently being evaluated in clinical trials. However, the mechanisms by which BRD4 and DOT1L regulate leukaemogenic transcription programs remain unclear. Using quantitative proteomics, chemoproteomics and biochemical fractionation we find that native BRD4 and DOT1L exist in largely separate protein complexes. Genetic disruption or small molecule inhibition of BRD4 and DOT1L shows marked synergistic activity against MLL-FP leukaemia cell lines, primary human leukaemia cells and murine leukaemia models. Mechanistically, we find a previously unrecognised functional collaboration between DOT1L and BRD4 that is especially important at highly transcribed genes in close proximity to superenhancers. DOT1L via H3K79me2 facilitates the deposition of histone H4 acetylation, which in turn regulates the binding of BRD4 to chromatin. These data provide novel insights into the regulation of transcription and specify a molecular framework for therapeutic intervention in this poor prognostic disease. Overall design: RNASeq of MV4;11 cells transduced with scramble shRNA or BRD4 shRNA in combination with DMSO or SGC0946 in triplicate

Publication Title

Functional interdependence of BRD4 and DOT1L in MLL leukemia.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP074419
RNASeq of MLL-AF9 cells transduced with scramle shRNA or BRD4 shRNA in combination with DMSO or SGC0946
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Central to the molecular pathogenesis of MLL leukaemia is the abnormal co-optation of members of transcription complexes including disrupter of telomeric silencing 1-like (DOT1L) and bromodomain containing protein 4 (BRD4). Consequently, targeted therapies against DOT1L and BRD4 are currently being evaluated in clinical trials. However, the mechanisms by which BRD4 and DOT1L regulate leukaemogenic transcription programs remain unclear. Using quantitative proteomics, chemoproteomics and biochemical fractionation we find that native BRD4 and DOT1L exist in largely separate protein complexes. Genetic disruption or small molecule inhibition of BRD4 and DOT1L shows marked synergistic activity against MLL-FP leukaemia cell lines, primary human leukaemia cells and murine leukaemia models. Mechanistically, we find a previously unrecognised functional collaboration between DOT1L and BRD4 that is especially important at highly transcribed genes in close proximity to superenhancers. DOT1L via H3K79me2 facilitates the deposition of histone H4 acetylation, which in turn regulates the binding of BRD4 to chromatin. These data provide novel insights into the regulation of transcription and specify a molecular framework for therapeutic intervention in this poor prognostic disease. Overall design: RNASeq of MLL-AF9 cells transduced with scramle shRNA or BRD4 shRNA in combination with DMSO or SGC0946 in triplicate

Publication Title

Functional interdependence of BRD4 and DOT1L in MLL leukemia.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon SRP062099
RNASeq of MV4;11 cell treated with DMSO, I-BET, SGC0946 and combination of I-BET and SGC0946
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Central to the molecular pathogenesis of MLL leukaemia is the abnormal co-optation of members of transcription complexes including disrupter of telomeric silencing 1-like (DOT1L) and bromodomain containing protein 4 (BRD4). Consequently, targeted therapies against DOT1L and BRD4 are currently being evaluated in clinical trials. However, the mechanisms by which BRD4 and DOT1L regulate leukaemogenic transcription programs remain unclear. Using quantitative proteomics, chemoproteomics and biochemical fractionation we find that native BRD4 and DOT1L exist in largely separate protein complexes. Genetic disruption or small molecule inhibition of BRD4 and DOT1L shows marked synergistic activity against MLL-FP leukaemia cell lines, primary human leukaemia cells and murine leukaemia models. Mechanistically, we find a previously unrecognised functional collaboration between DOT1L and BRD4 that is especially important at highly transcribed genes in close proximity to superenhancers. DOT1L via H3K79me2 facilitates the deposition of histone H4 acetylation, which in turn regulates the binding of BRD4 to chromatin. These data provide novel insights into the regulation of transcription and specify a molecular framework for therapeutic intervention in this poor prognostic disease. Overall design: RNASeq of MV4;11 cell treated with DMSO, I-BET, SGC0946 and combination of I-BET and SGC0946 in duplicate

Publication Title

Functional interdependence of BRD4 and DOT1L in MLL leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP074418
RNASeq of 4SU labelled nascent RNA in MV4;11 cell treated with DMSO, I-BET, SGC0946 and combination of I-BET and SGC0946
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Central to the molecular pathogenesis of MLL leukaemia is the abnormal co-optation of members of transcription complexes including disrupter of telomeric silencing 1-like (DOT1L) and bromodomain containing protein 4 (BRD4). Consequently, targeted therapies against DOT1L and BRD4 are currently being evaluated in clinical trials. However, the mechanisms by which BRD4 and DOT1L regulate leukaemogenic transcription programs remain unclear. Using quantitative proteomics, chemoproteomics and biochemical fractionation we find that native BRD4 and DOT1L exist in largely separate protein complexes. Genetic disruption or small molecule inhibition of BRD4 and DOT1L shows marked synergistic activity against MLL-FP leukaemia cell lines, primary human leukaemia cells and murine leukaemia models. Mechanistically, we find a previously unrecognised functional collaboration between DOT1L and BRD4 that is especially important at highly transcribed genes in close proximity to superenhancers. DOT1L via H3K79me2 facilitates the deposition of histone H4 acetylation, which in turn regulates the binding of BRD4 to chromatin. These data provide novel insights into the regulation of transcription and specify a molecular framework for therapeutic intervention in this poor prognostic disease. Overall design: RNASeq of 4SU labelled nascent RNA in MV4;11 cell treated with DMSO, I-BET, SGC0946 and combination of I-BET and SGC0946 in duplicate

Publication Title

Functional interdependence of BRD4 and DOT1L in MLL leukemia.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP128647
Dazl maintains proliferating germ cells through a network of polyA-proximal mRNA interactions [Spermatogonia PolyA-Seq]
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Dazl (deleted in azoospermia like) is a member of the DAZ family of germ cell-restricted RNA binding proteins required for gametogenesis from worm to human. The direct RNA targets and functions of these essential proteins are poorly understood. Here, we generated high-resolution, transcriptome-wide maps of Dazl-RNA interactions in mouse testes. These maps provide important insights into the mechanism of Dazl recruitment to mRNA and reveal Dazl binding to thousands of mRNAs predominantly through sequence-specific interactions near the polyA tail. Using transgenic mice and fluorescence activated cell sorting (FACS), we isolated DAZL knockout germ cells and used RNA-Seq to identify mRNAs sensitive to DAZL-ablation. Intersecting the RNA-Seq and Dazl-RNA interaction datasets revealed that Dazl enhances expression of a subset of directly-bound transcripts, namely mRNAs for a network of essential cell cycle regulatory genes. Collectively, our integrative analysis delineates a Dazl-dependent post-transcriptional gene regulatory program essential for mammalian germ cell maintenance. Overall design: PolyA Seq libraries generated from isolated spermatogonial cells

Publication Title

DAZL Regulates Germ Cell Survival through a Network of PolyA-Proximal mRNA Interactions.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples

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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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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