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accession-icon SRP018221
RNA-sequencing (RNA-seq) in breast cancer cell lines after ectopic manipulation of miR-26a expression
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-26a in both MCF-7 and MDA-MB-231 breast cancer cell lines. Overall design: To evaluate the entire set of genes modulated by miR-26a in breast cancer, we performed RNA-seq after ectopic manipulation of this miRNA. We over-expressed miR-26a in MCF-7 epithelial cancer cell lines and also reduced its activity by stably transfecting MDA-MB-231 mesenchymal-like cancer cell lines with a specific sponge vector. GO terms and pathway enriched analysis of the transcripts that significantly change upon miR-26 ectopic manipulation implicates miR-26ab in cell cycle, apoptosis, cell spreading and cell adhesion in breast cancer

Publication Title

Sustained expression of miR-26a promotes chromosomal instability and tumorigenesis through regulation of CHFR.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE27833
Notch signaling in HSC
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE27811
Expression data from LSK WT, GMP WT and GMP NcstnKO
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE27799
Expression data from LSK WT and LSK N1-C+
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE27794
Expression data from LSK WT and LSK NcstnKO
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE20667
The Notch/Hes1 pathway sustains NF-B activation through CYLD repression in T cell leukemia
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The NF-B pathway is a critical regulator of the immune system and has been implicated in cellular transformation and tumorigenesis. NF-B response is regulated by the activation state of the IB kinase (IKK) complex and triggered by a wide spectrum of stimuli. We previously reported that NF-B is downstream of Notch1 in T cell acute lymphoblastic leukaemia (T-ALL), however both the mechanisms involving Notch1-induced NF-B activation and the potential importance of NF-B in the maintenance of the disease are unknown. Here we visualize Notch-induced NF-B activation using both human T-ALL cell lines and animal models of this type of leukemia. We show that it is not Notch1 itself but Hes1, a canonical Notch target, the responsible for sustaining IKK activation in T-ALL. Hes1 exerts its effects by a direct transcriptional repression of the deubiquitinating enzyme CYLD, a well-characterized IKK inhibitor. Consistently, CYLD expression is significantly reduced in primary T-ALL leukemias. Finally, we demonstrate that IKK complex inhibition is a promising option for the targeted therapy of T-ALL as suppression of IKK function affected both the survival of human T-ALL cells in vitro and the maintenance of the disease in vivo.

Publication Title

The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE53201
Expression data from human coronary artery endothelial cells treated with HDL components
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We quantified differential gene (mRNA) expression in human coronary artery cells treated with native HDL, reconstituted HDL, lipid-free apolipoprotein A-I, small unilamellar vesicles, or PBS control.

Publication Title

HDL-transferred microRNA-223 regulates ICAM-1 expression in endothelial cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE87490
Amygdalar microRNA-15a is essential for coping with chronic stress
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Amygdalar MicroRNA-15a Is Essential for Coping with Chronic Stress.

Sample Metadata Fields

Specimen part

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accession-icon GSE53605
Molecular Profiles Associated with Calcineurin Inhibitor Toxicity Post-Kidney Transplant: Input to Chronic Allograft Dysfunction
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The molecular basis of calcineurin inhibitor toxicity (CNIT) in kidney transplantation (KT) and its contribution to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA) were evaluated.

Publication Title

Evaluation of molecular profiles in calcineurin inhibitor toxicity post-kidney transplant: input to chronic allograft dysfunction.

Sample Metadata Fields

Specimen part

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accession-icon GSE60187
Evaluation of Niacinamide effects on murine primary macrophage transcriptional regulation and cell cycle progression.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Murine MafB/c-MAF double KO (Maf-DKO) primary macrophages are known for their unlimited non-tumorigenic self-renewal ability (Aziz et al., 2009). In an in vitro screen for cytokines and small molecules we identified Niacinamide (NAM) a potent inhibitor of their proliferative potential characterized by a reversible cell cycle arrest.

Publication Title

SIRT1 regulates macrophage self-renewal.

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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