refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 1117 results
Sort by

Filters

Technology

Platform

accession-icon GSE18015
Molecular analysis of ex-vivo CD133+ GBM cells revealed a common invasive and angiogenic profile but different proliferative signatures among high grade gliomas.
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Gliomas are the most common type of primary brain tumours, and in this group glioblastomas (GBMs) are the higher-grade gliomas with fast progression and unfortunate prognosis. Two major aspects of glioma biology that contributes to its awful prognosis are the formation of new blood vessels through the process of angiogenesis and the invasion of glioma cells. Despite of advances, two-year survival for GBM patients with optimal therapy is less than 30%. Even in those patients with low-grade gliomas, that imply a moderately good prognosis, treatment is almost never curative. Recent studies have demonstrated the existence of a small fraction of glioma cells with characteristics of neural stem cells which are able to grow in vitro forming neurospheres and that can be isolated in vivo using surface markers such as CD133. The aim of this study was to define the molecular signature of GBM cells expressing CD133 in comparison with non expressing CD133 cells. This molecular classification could lead to the finding of new potential therapeutic targets for the rationale treatment of high grade GBM.

Publication Title

Molecular analysis of ex-vivo CD133+ GBM cells revealed a common invasive and angiogenic profile but different proliferative signatures among high grade gliomas.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon SRP055108
Global Gene Expression analysis of CUTLL1 cell lines after treatment with Perhexiline
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We identify perhexiline, a small molecule inhibitor of mitochondrial carnitine palmitoyltransferase-1, as a HES1-signature antagonist drug with robust antileukemic activity against NOTCH1 induced leukemias in vitro and in vivo. Overall design: RNA-Seq from CUTLL1 cell lines treated with Perhexiline or vehicle for 3 days

Publication Title

Therapeutic targeting of HES1 transcriptional programs in T-ALL.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP149483
RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the reporter gene LacZ (located next to the oncogene in the same polycistronic mRNA), by loading CD31-/CD45- pneumocytes with the LacZ-activated fuorogenic molecule FDG prior to FACS sorting. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.

Publication Title

Sirt1 protects from K-Ras-driven lung carcinogenesis.

Sample Metadata Fields

Subject

View Samples
accession-icon SRP149487
RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen and 2 weeks of chase
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment plus 2 weeks without tamoxifen. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the fluorescent reporter gene Katushka (located at an independent locus), by detecting Katushka fluorescence. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.

Publication Title

Sirt1 protects from K-Ras-driven lung carcinogenesis.

Sample Metadata Fields

Sex, Subject

View Samples
accession-icon GSE3541
DNA microarray reveals novel genes induced by mechanical forces in fetal lung type II epithelial cells
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Mechanical forces are essential for normal fetal lung development. However, the cellular and molecular mechanisms regulating this process remain largely unknown. In the present study, we used oligonucleotide microarray technology to investigate gene expression profile in cultured E19 rat fetal lung type II epithelial cells exposed to a level of mechanical strain similar to that observed in utero. Significance Analysis of Microarrays (SAM) identified 92 genes differentially expressed by strain. Interestingly, several members of the solute carrier family of amino acid transporters, genes involved in amino acid synthesis and development, and amiloride-sensitive epithelial sodium channel gene were induced by strain. These results were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Thus, this study identifies genes induced by strain that may be important for amino acid signaling pathways, protein synthesis and development in fetal type II cells. In addition, these data suggest that mechanical forces may contribute to facilitate lung fluid reabsorption in preparation for birth. Taken together, the present investigation provides further insights into how mechanical forces may modulate fetal lung development.

Publication Title

DNA microarray reveals novel genes induced by mechanical forces in fetal lung type II epithelial cells.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE13902
BW25113 fhlA/pCA24N-FhlA133 vs fhlA/pCA24N-FhlA in modified-complex 20 mM formate at 37C
  • organism-icon Escherichia coli
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Variant FhlA133 (Q11H, L14V, Y177F, K245R, M288K, and I342F) had eight- fold higher hydrogen production than FhlA wild-type under 30 min of anaerobic incubation in modified-complex 20 mM formate at 37C. The mechanism by which the FhlA133 mutations increase hydrogen production is by increasing the transcription of all of the genes activated by the native FhlA (FHL complex).

Publication Title

Protein engineering of the transcriptional activator FhlA To enhance hydrogen production in Escherichia coli.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP045460
CXCL12/CXCR4 signaling mediates niche occupancy and tumor maintenance in T-cell leukemia
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy characterized by infiltration of the bone marrow and other sites with transformed T cell progenitors. The role of tissue microenvironments in the pathogenesis of T-ALL or any other type of acute leukemia is little understood. In delineating interactions between T-ALL cells and their environment, we initially found that T-ALL cells express high surface levels of the chemokine receptor CXCR4. Intravital imaging of an intact tibia revealed T-ALL cells in direct contact with bone marrow stromal cells producing the CXCR4 ligand, CXCL12. Genetic targeting of CXCR4 on T-ALL cells resulted in a marked reduction of leukemia burden and prolonged disease remission, and disruption of the CXCL12/CXCR4 axis using small molecule inhibitors prevented T-ALL progression in a primary xenograft model. Finally, we were able to show that CXCR4 inhibition significantly decreased expression of Myc and its target genes. Myc expression is a key regulator of T-ALL leukemia initiating cell (LIC) activity, suggesting that CXCR4 inhibition can suppress LIC activity by silencing the Myc response in T-ALL cells. Our data suggest that targeting of CXCL12/CXCR4 signaling could be a powerful new tool for combating T-ALL, a disease with no current targeted therapies. Overall design: Mouse T-ALL cells were treated ex vivo with Cxcr4 inhibitor AMD3100 or vehicle control. Additionally, mouse T-ALL primary tumors were isolated from control (Cxcr4+/+) or knockout (Cxcr4-/-) animals. Total RNA was extracted from samples using the RNeasy Plus Mini Kit (Qiagen). Samples were then subject to PolyA selection using oligo-dT beads (Life Technologies, Carlsbad, CA) according to the manufacturer''s instructions. The resulting RNA samples were then used as input for library construction using the dUTP method as described by Parkhomchuck et al., 2009. RNA libraries were then sequenced on the Illumina HiSeq 2500 using 50bp single-end reads.

Publication Title

CXCL12-Producing Vascular Endothelial Niches Control Acute T Cell Leukemia Maintenance.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE35014
Discovery of genes regulated by the metastasis suppressor gene, RhoGDI2
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A number of studies find that metastasis suppressor proteins, including RhoGDI2, may function in part though controlling expression of genes regulating metastasis (reviewed in Smith and Theodorescu, Nature Reviews Cancer, 2009, PMID: 19242414). To uncover systematically gene expression patterns dependent on RhoGDI2 expression, we profiled gene expression in stably transfected control (GFP empty vector) UM-UC-3 bladder carcinoma cells (which have lost endogenous expression of RhoGDI2, as occurs commonly in the progression of bladder cancer PMID: 15173088), as well as stably transfected GFP-tagged RhoGDI2 expressing UM-UC-3 cells.

Publication Title

RhoGDI2 suppresses lung metastasis in mice by reducing tumor versican expression and macrophage infiltration.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP071313
Analysis of differential gene expression in Drosophila dIME4 null mutants [single-end]
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Methylation of mRNA at the N6 position of adenosin is known for a long time, but its function remains poorly understood. Here generated a null mutant in the catalytic subunit of the m6A mRNA methylosome, dIME4, in Drosophila to determine the impact of loss of m6A on gene expression using Illumina sequencing. Overall design: Since dIME4 is preferentially expressed in the nervous system and dIME4 null mutants are viable, we compared gene expression and alternative splicing in wild type (2 samples) and dIME4 mutants (3 samples) with genetic background matched w control females in neuron enriched head/thorax.

Publication Title

m<sup>6</sup>A potentiates Sxl alternative pre-mRNA splicing for robust Drosophila sex determination.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP071302
Analysis of differential gene expression in Drosophila dIME4 null mutants [paired-end]
  • organism-icon Drosophila melanogaster
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Methylation of mRNA at the N6 position of adenosin is known for a long time, but its function remains poorly understood. Here generated a null mutant in the catalytic subunit of the m6A mRNA methylosome, dIME4, in Drosophila to determine the impact of loss of m6A on gene expression using Illumina sequencing. Overall design: Since dIME4 is preferentially expressed in the nervous system and dIME4 null mutants are viable, we compared gene expression and alternative splicing in wild type (2 samples) and dIME4 mutants (3 samples) with genetic background matched w control females in neuron enriched head/thorax.

Publication Title

m<sup>6</sup>A potentiates Sxl alternative pre-mRNA splicing for robust Drosophila sex determination.

Sample Metadata Fields

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact