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accession-icon GSE50603
Effect of L-Proline on mouse embryonic stem cells (ESCs)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that the non-essential amino acid L-Proline (L-Pro) acts as a signaling molecule that promotes the conversion of embryonic stem cells (ESCs) into mesenchymal-like, spindle-shaped, highly motile, invasive pluripotent stem cells. This embryonic stem cell-to-mesenchymal-like transition (esMT) is accompanied by a genome-wide remodeling of the transcriptome

Publication Title

L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation.

Sample Metadata Fields

Cell line

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accession-icon SRP052064
Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells following Ikaros restoration
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. Overall design: RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells isolated from two untreated and two 3-day Dox-treated mice.

Publication Title

Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP052063
Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells following Ikaros restoration
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. Overall design: RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells isolated from three untreated and three 3-day Dox-treated mice. There were two sequencing runs of each RNA sample.

Publication Title

Activated Notch counteracts Ikaros tumor suppression in mouse and human T-cell acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE42261
Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Notch pathway activation targets AML-initiating cell homeostasis and differentiation.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

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accession-icon GSE42259
Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation: THP1 cell line
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation.

Publication Title

Notch pathway activation targets AML-initiating cell homeostasis and differentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE42260
Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation: MLL-AF9 transformed LGMP
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To determine role of Notch signaling in AML leukemia initiating cells we used a conditional mouse knock-in model of Notch1-IC to induce Notch1-IC expression in MLL-AF9 transformed LGMP. WT and Notch1-IC+ LGMP were analyzed to determined genes controlled by Notch signaling.

Publication Title

Notch pathway activation targets AML-initiating cell homeostasis and differentiation.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP033415
Expression profiling of mouse bone marrow pre-B cells
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Triplicate RNA-seq expression analysis of bone marrow pre-B cells isolated from mice, to demonstrate repertoire at the IgH locus Overall design: Triplicate RNA-seq expression analysis of bone marrow pre-B cells

Publication Title

Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP041820
Inducible PAX5 expression in a human B lymphoblastic leukemia cell line
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Hypomorphic mutations of the transcription factor PAX5 occur in one third of B-progenitor acute lymphoblastic leukemias (B-ALLs). To identify PAX5-regulated genes in B-ALL, here we employ inducible expression of PAX5 in a human B-ALL cell line (REH) that harbors a loss-of-function mutation in PAX5. In this model, inducing PAX5 expression is associated with competitive disadvantage. Overall design: Comparison of REH cell lines with Dox-inducible expression of PAX5-IRES-GFP, or control GFP alone. GFP positive cells were isolated by FACS.

Publication Title

Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062844
Gene expression profiling from cohesin knockdown cells obtained grown in methylcellulose
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed RNA-sequencing in c-Kit+ cells that were infected with retroviruses expressing shRNAs for Renilla, Rad21, Smc1a, Smc3 or Stag2. These cells were grown in methylcellulose (M3434) for either one passage (P1) or replated for five passages (P5). Overall design: RNA-sequencing control (Ren) and cohesin (Rad21, Smc1a, Smc3 and Stag2) knockdown cells.

Publication Title

Cohesin loss alters adult hematopoietic stem cell homeostasis, leading to myeloproliferative neoplasms.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP062845
Gene expression profiling of control cohesin knockdown LSK cells
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed RNA-sequencing in LSK cells (Lin(neg)/c-Kit(+)/Sca-1(+)) from shRNA mice carrying an shRNA for Renilla, Smc1a or Stag2. Overall design: RNA-sequencing control (Renilla) and cohesin (Smc1a and Stag2) knockdown cells.

Publication Title

Cohesin loss alters adult hematopoietic stem cell homeostasis, leading to myeloproliferative neoplasms.

Sample Metadata Fields

Specimen part, 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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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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