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accession-icon GSE64536
STAT3 knockdown during transformation
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

siSTAT3 knockdown of a tamoxifen initiated, transformation inducible, breast cancer model system (MCF10A-ER-Src), with associated controls of EtOH and siNEG treatments.

Publication Title

STAT3 acts through pre-existing nucleosome-depleted regions bound by FOS during an epigenetic switch linking inflammation to cancer.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE1428
Skeletal muscle sarcopenia
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This series includes the global gene expression profile of the vastus lateralis muscle for 10 young (19-25 years old) and 12 older (70-80 years old) male subjects.

Publication Title

Identification of a molecular signature of sarcopenia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP076334
Identification of rare, dormant and therapy resistant stem cells in acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 228 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Tumor relapse is associated with dismal prognosis, but responsible biological principles remain incompletely understood. To isolate and characterize relapse-inducing cells, we used genetic engineering and proliferation-sensitive dyes in patient-derived xenografts of acute lymphoblastic leukemia (ALL). We identified a rare subpopulation that resembled relapse-inducing cells with combined properties of long-term dormancy, treatment resistance, and stemness. Single-cell and bulk expression profiling revealed their similarity to primary ALL cells isolated from pediatric and adult patients at minimal residual disease (MRD). Therapeutically adverse characteristics were reversible, as resistant, dormant cells became sensitive to treatment and started proliferating when dissociated from the in vivo environment. Our data suggest that ALL patients might profit from therapeutic strategies that release MRD cells from the niche. Overall design: Gene expression profiles from two PDX ALL Samples (ALL-199 & ALL-265) were generated for either dormant (LRC) vs. dividing (non-LRC) cells or drug treated vs. non-treated cells. For single cell analysis one mouse were analyzed for each condition.

Publication Title

Characterization of Rare, Dormant, and Therapy-Resistant Cells in Acute Lymphoblastic Leukemia.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP091696
JNK promotes epithelial cells anoikis by transcriptional and post-translational regulation of BH3-only proteins
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Developmental morphogenesis, tissue injury, and oncogenic transformation can cause the detachment of epithelial cells. These cells are eliminated by a specialized form of apoptosis (anoikis). While the processes that contribute to this form of cell death have been studied, the underlying mechanisms remain unclear. Here we tested the role of the cJUN NH2-terminal kinase (JNK) signaling pathway using murine models with compound JNK-deficiency in mammary and kidney epithelial cells. These studies demonstrated that JNK is required for efficient anoikis in vitro and in vivo. Moreover, JNK-promoted anoikis required pro-apoptotic members of the BCL2 family of proteins. We show that JNK acts through a BAK/BAX-dependent apoptotic pathway by increasing BIM expression and phosphorylating BMF leading to death of detached epithelial cells. Overall design: In order to understand the role of the JNK pathway in anoikis, Rosa-CreER (Control) and Jnk1flox/flox Jnk2-/- Rosa-CreER (Jnk1-/-Jnk2-/-) cells were grown as attached monoloayers or suspended for 4 hours. RNA was isolated from these cells and subjected to RNASeq to measure differential gene expression. Three separate samples from each condition were analyzed.

Publication Title

JNK Promotes Epithelial Cell Anoikis by Transcriptional and Post-translational Regulation of BH3-Only Proteins.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP034750
Identification of small ORFs in vertebrates using ribosome footprinting and evolutionary conservation
  • organism-icon Danio rerio
  • sample-icon 622 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Identification of the coding elements in the genome is a fundamental step to understanding the building blocks of living systems. Short peptides (< 100 aa) have emerged as important regulators of development and physiology, but their identification has been limited by their size. We have leveraged the periodicity of ribosome movement on the mRNA to define actively translated ORFs by ribosome footprinting. This approach identifies several hundred translated small ORFs in zebrafish and human. Computational prediction of small ORFs from codon conservation patterns corroborates and extends these findings and identifies conserved sequences in zebrafish and human, suggesting functional peptide products (micropeptides). These results identify micropeptide-encoding genes in vertebrates, providing an entry point to define their function in vivo. Overall design: Ribosome profiling experiments at five timepoints across zebrafish development in WT embryos

Publication Title

Upstream ORFs are prevalent translational repressors in vertebrates.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP010040
Ribosome profiling of early zebrafish embryos -- miRNA-mediated regulation during embryogenesis causes translational repression before mRNA decay
  • organism-icon Danio rerio
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

MicroRNAs regulate gene expression through deadenylation, repression and mRNA decay. However, the contribution of each mechanism in non-steady-state situations remains unclear. We monitored the impact of miR-430 on ribosome occupancy of endogenous mRNAs in wild type and dicer mutants lacking mature miR-430. Our results indicate that miR-430 reduces the number of ribosomes on target mRNAs before causing mRNA decay. Translational repression occurs before complete deadenylation, and disrupting deadenylation using an internal poly(A) tail did not block target repression. Finally, we observe that ribosome density along the length of the target mRNA remains constant, suggesting that translational repression occurs by reducing the initiation rate rather than reducing elongation or causing ribosomal drop-off. In summary, our results show that miR-430 regulates translation initiation before inducing mRNA decay. Overall design: Time course parallel ribosome profiling and input mRNA quantification in wildtype and MZdicer mutant embryos

Publication Title

Ribosome profiling shows that miR-430 reduces translation before causing mRNA decay in zebrafish.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26079
Genome-wide analysis gene expression in SUM-149 cells expressing AREG shRNA
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Results of knocking-down AREG expression in SUM-149 cells by lenitviral infection of shRNA vectors and measuring gene expression provides information as to what genes are regulated by AERG in inflammatory breast cancer cells.

Publication Title

Knock-down of amphiregulin inhibits cellular invasion in inflammatory breast cancer.

Sample Metadata Fields

Disease, Disease stage, Cell line

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accession-icon E-MEXP-152
Transcription profiling of response of adult Drosophila to oxidative and ER stress
  • organism-icon Drosophila melanogaster
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

We used oligonucleotide microarrays to address the specificities of transcriptional responses of adult Drosophila to different stresses induced by paraquat and H2O2, two oxidative stressors, and by tunicamycin which induces an endoplasmic reticulum (ER) stress. Flies were tested 24 hours after exposure to continuous stresses induced by ingestion of paraquat, H2O2 or tunicamycin at concentrations leading to similar effects on viability. We used concentrations of 1% H2O2, 5mM paraquat and 12uM of tunicamycin which lead to negligeable mortality at 24 hours. A paraquat concentration of 15mM was also used for comparison with previous studies Both specific and common responses to the three stressors were observed and whole genome functional analysis identified several important classes of stress responsive genes. Within some functional classes, we observed large variabilities of transcriptional changes between isozymes, which may reflect unsuspected functional specificities.

Publication Title

Genome wide analysis of common and specific stress responses in adult drosophila melanogaster.

Sample Metadata Fields

Sex, Age, Compound, Time

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accession-icon GSE13833
Transcriptome changes triggered by the synthetic defense elicitors DCA and INA in Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

DCA (3,5-Dichloroanthranilic acid) is a newly identified synthetic defense elicitor. To perform a comparative analysis of defense responses triggered by DCA and the structurally related defense inducer INA (2,6-Dichloroisonicotinic acid) Affymetrix chip experiments were performed with Arabidopsis thaliana seedlings treated with one of these two compounds.

Publication Title

The synthetic elicitor 3,5-dichloroanthranilic acid induces NPR1-dependent and NPR1-independent mechanisms of disease resistance in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE29625
Human embryonic stem cells derived from embryos at different stages of development share similar transcription profiles
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have derived hESC from biopsied blastomeres of cleavage stage embryos under virtually the same conditions we used for the derivation of hESC lines from inner cell mass of blastocyst stage embryos. Blastomere-derived hESC lines exhibited all the standard characteristics of hESC including undifferentiated proliferation, genomic stability, expression of pluripotency markers and the ability to differentiate into the cells of all three germ layers both in vitro and in vivo. To examine whether hESC lines derived from two developmental stages of the embryo differ in gene expression, we have subjected three blastomere-derived hESC lines and two ICM-derived hESC lines grown under identical culture conditions to transcriptome analysis using gene expression arrays. Unlike previously reported comparisons of hESC lines which demonstrated, apart from core hESC-associated pluripotency signature, significant variations in gene expression profiles of different lines, our data show that hESC lines derived and grown under well-controlled defined culture conditions adopt nearly identical gene expression profiles. Moreover, blastomere-derived and ICM-derived hESC exhibited very similar transcriptional profiles independent of the developmental stage of the embryo from which they originated. Furthermore, this profile was evident in very early passages of the cells and did not appear to be affected by extensive passaging. These results suggest that during derivation process cells which give rise to hESC acquire virtually identical stable phenotype and are not affected by the developmental stage of the starting cell population.

Publication Title

Human embryonic stem cells derived from embryos at different stages of development share similar transcription profiles.

Sample Metadata Fields

Specimen part, Disease, Cell line

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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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