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accession-icon GSE27648
Expression profile of Maize (Zea mays L.) Embryonic Axes During Germination: Regulation of Ribosomal Protein mRNAs.
  • organism-icon Zea mays
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Seed germination is a critical developmental process in plant propagation. Knowledge of the gene expression patterns in this critical process is important in order to understand the main biochemical reactions involved in successful germination, specially for economically relevant plants such as Maize.

Publication Title

Expression profile of maize (Zea mays L.) embryonic axes during germination: translational regulation of ribosomal protein mRNAs.

Sample Metadata Fields

Treatment, Time

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accession-icon SRP101670
Ablation of the stress protease OMA1 protects against heart failure
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. Here we evaluate three different models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction, and LV myocardial ischemia and hypertrophy. Regardless of whether LVEF is preserved or reduced, our results indicate that the three models share common molecular features: an increase in mitochondrial ROS, followed by ultrastructural alterations in the mitochondrial cristae and loss of mitochondrial integrity that lead to cardiomyocyte death. We show that the ablation of the mitochondrial protease OMA1 averts cardiomyocyte death in all three experimental HF models, and thus, plays a direct role in cardiomyocyte protection. This finding identifies OMA1 as a potential target for preventing the progression of myocardial damage in HF associated to a variety of etiologies. Overall design: Transcriptome analysis of 12-week-old wild type mice versus OMA1 KO mice under control (non-treated) or treated with Isoproterenol chronically (implanted minipumps) for 7 days in heart tissue. The nuclear genetic background for both genotypes is C57BL/6JOlaHsd.

Publication Title

Ablation of the stress protease OMA1 protects against heart failure in mice.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Subject

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accession-icon SRP062067
Telomerase is essential for zebrafish heart regeneration
  • organism-icon Danio rerio
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction. Overall design: Heart transcriptomes of WT and telomerase defective adult zebrafish animals were profiled by RNASeq, in control conditions and 3 days after heart cryoinjury.

Publication Title

Telomerase Is Essential for Zebrafish Heart Regeneration.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19592
DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

DUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To understand more about the cellular responses regulated by DUSP1 in NSCLC cells, we interfered DUSP1 expression in the NSCLC cell line H460 and studied the changes in gene expression differentially regulated by this phosphatase.

Publication Title

DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small-cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE154589
Inhibition of Inflammatory Signaling in Pax5 Mutant Cells Mitigates B-cell leukemogenesis against leukemia
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We used microarrays to investigate gene expression changes in healthy and leukemic cells from Pax5+/- and IL6+/-;Pax5+/- mice in CF and SPF housing conditions.

Publication Title

Inhibition of inflammatory signaling in Pax5 mutant cells mitigates B-cell leukemogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE83572
LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche
  • organism-icon Mus musculus
  • sample-icon 42 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

Lmo2 expression defines tumor cell identity during T-cell leukemogenesis.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

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accession-icon SRP128585
Von Hippel-Lindau protein is required for optimal alveolar macrophage terminal differentiation, self-renewal and function.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The rapid transit from hypoxia to normoxia in the lung that follows the first breath in newborn mice coincides with alveolar macrophage (AM) differentiation. However, whether sensing of oxygen affects AM maturation and function has not been previously explored. We have generated mice whose AMs show a deficient ability to sense oxygen after birth by deleting Vhl, a negative regulator of HIF transcription factors, in the CD11c compartment (CD11c?Vhl mice). VHL-deficient AMs show an immature-like phenotype and an impaired self-renewal capacity in vivo that persists upon culture ex vivo. VHL-deficient phenotype is intrinsic in AMs derived from monocyte precursors in mixed bone marrow chimeras. Moreover, unlike control Vhlfl/fl, AMs from CD11c?Vhl mice do not revert pulmonary alveolar proteinosis when transplanted into Csf2rb-/- mice, demonstrating that VHL contributes to AM-mediated surfactant clearance. Thus, our results suggest that optimal AM terminal differentiation, self-renewal, and homeostatic function requires their oxygen sensing capacity. Overall design: BAL AMs were pooled from 5-7 age and sex-matched mice per genotype and further purified by positive selection with anti-CD11c-microbeads (Miltenyi Biotec), following manufacturer's instructions. Cell lysis was performed with buffer RLT (Qiagen), containing 10µ/ml ß-mercaptoethanol and RNA was isolated with RNeasy Plus Mini Kit (Qiagen). RNA concentration and integrity were determined with an Agilent 2100 Bioanalyzer (Caliper Life Science). Samples with RNA integrity values > 8 were further processed. A total of 3 pools per genotype were used for RNA Seq.

Publication Title

Von Hippel-Lindau Protein Is Required for Optimal Alveolar Macrophage Terminal Differentiation, Self-Renewal, and Function.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP044736
Deficiency in glucose transporter 12 results in heart failure and a diabetic phenotype in zebrafish
  • organism-icon Danio rerio
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Cardiomyopathies-associated metabolic pathologies (e.g. T2D and insulin resistance) are a leading cause of mortality. It is known that the association between the pathologies works in both directions, where heart failure can lead to metabolic derangements such as insulin resistance. This intricate crosstalk exemplifies the importance of a fine coordination between one of the most energy demanding organs and an equilibrated carbohydrate metabolism. In this light, to assist in the understanding of the role of insulin regulated glucose transporters and the development of cardiomyopathies, we set out to study GLUT12. GLUT12 is a novel insulin regulated GLUT expressed in the main insulin sensitive tissues such as cardiac and skeletal muscle and adipose tissue. This study investigates the role of GLUT12 in heart failure and diabetes by developing a model for glut12 deficiency in zebrafish. Overall design: 6 samples in total were analyzed. 3 replicates from control samples (injected with contol MO) and 3 replicates from glut12 morphant samples (injected with glut12 splice MO). In each sample 10 embryos were pooled.

Publication Title

GLUT12 deficiency during early development results in heart failure and a diabetic phenotype in zebrafish.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE134614
Expression data from betalains treated C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconAffymetrix C. elegans Gene 1.1 ST Array

Description

Effects of betalains in C. elegans gene expression is studied, as our previous results showed a lifespan extension effect produced by theses molecules

Publication Title

Betalain health-promoting effects after ingestion in Caenorhabditis elegans are mediated by DAF-16/FOXO and SKN-1/Nrf2 transcription factors.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE20935
Gene expression in NKR-P1B+ versus Ly49s3+ rat NK cells
  • organism-icon Rattus norvegicus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Two major subsets of rat natural killer (NK) cells can be distinguished based on their expression of either the Ly49s3 or the NKR-P1B lectin-like receptor. Ly49s3+ NK cells, but not NKR-P1B+ NK cells, express a wide range of Ly49 receptors.

Publication Title

Two complementary rat NK cell subsets, Ly49s3+ and NKR-P1B+, differ in phenotypic characteristics and responsiveness to cytokines.

Sample Metadata Fields

Specimen part

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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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