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accession-icon GSE12214
Microcystin Genomic Effects on Zebrafish Larvae
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

Zebrafish (Danio rerio) were obtained from the Zebrafish Research Facility maintained in the Center for Environmental Biotechnology at the University of Tennessee. Fish husbandry, spawning, and experimental procedures were conducted with approval from the University of Tennessee Institutional Animal Care and Use Committee (Protocol #1690-1007). Water for holding fish and conducting experiments (hereafter referred to as fish water) consisted of MilliQ water (Millipore, Bedford, MA) with ions added: 19 mg/L NaHCO3, 1 mg/L sea salt (Instant Ocean Synthetic Sea Salt, Mentor, OH), 10 mg/L CaSO4, 10 mg/L MgSO4, 2 mg/L KCl. Embryos were obtained by spawning adult fish with no history of contaminant exposure. Fertilization of embryos took place at the same time ( 15 min.), such that larvae used in experiments were of similar age at the time of exposure. All activities (maintenance of adult fish, spawning, and experiments) were conducted in an environmental chamber with a temperature of 27 1 C and 14:10h light:dark photoperiod.

Publication Title

Global gene expression profiling in larval zebrafish exposed to microcystin-LR and microcystis reveals endocrine disrupting effects of Cyanobacteria.

Alternate Accession IDs

E-GEOD-12214

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE60905
Transcriptional hallmarks of heterogeneous neural stem cell niches of the subventricular zone.
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon

Description

Throughout postnatal life in mammals, neural stem cells (NSCs) are located in the subventricular zone (SVZ) of the lateral ventricles. The greatest diversity of neuronal and glial lineages they generate occurs during early postnatal life in a region-specific manner. In order to evaluate potential heterogeneity in the NSC pool, we microdissected the dorsal and lateral SVZ at different postnatal ages and isolated NSCs and their immediate progeny based on their expression of Hes5-EGFP/Prominin1 and Ascl1-EGFP, respectively. Whole genome comparative transcriptome analysis revealed transcriptional regulators as major hallmarks that sustain postnatal SVZ regionalization. Manipulation of single genes encoding for locally enriched transcription factors influenced NSC specification indicating that the fate of regionalized postnatal SVZ NSCs can be readily modified . These findings reveal functional heterogeneity of NSCs in the postnatal SVZ and provide targets to recruit region-specific lineages in regenerative contexts.

Publication Title

Transcriptional Hallmarks of Heterogeneous Neural Stem Cell Niches of the Subventricular Zone.

Alternate Accession IDs

E-GEOD-60905

Sample Metadata Fields

Specimen part

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accession-icon GSE64154
Expression data from Fbxl10 overexpressing 3T3-L1 cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Target genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed

Publication Title

The FBXL10/KDM2B scaffolding protein associates with novel polycomb repressive complex-1 to regulate adipogenesis.

Alternate Accession IDs

E-GEOD-64154

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE46443
Expression data from mouse cerebral cortex
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains

Publication Title

A novel genetic locus modulates infarct volume independently of the extent of collateral circulation.

Alternate Accession IDs

E-GEOD-46443

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE10598
Transcriptional profile of rapidly stimulated atrial myocytes: Conservation with human atrial fibrillation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Atrial fibrillation (AF) is a progressive arrhythmia for which current therapy is inadequate. During AF, rapid stimulation causes atrial remodeling that promotes further AF. The cellular signals that trigger this process remain poorly understood, however, and elucidation of these factors would likely identify new therapeutic targets. We have previously shown that immortalized mouse atrial (HL-1) myocytes subjected to 24 hr of rapid stimulation in culture undergo remodeling similar to that seen in animal models of atrial tachycardia (AT) and human AF. This preparation is devoid of confounding in vivo variables that can modulate gene expression (e.g., hemodynamics). Therefore, we investigated the transcriptional profile associated with early atrial cell remodeling. RNA was harvested from HL-1 cells cultured for 24 hr in the absence and presence of rapid stimulation and subjected to microarray analysis. Data were normalized using Robust Multichip Analysis (RMA), and genes exhibiting significant differential expression were identified using the Significance Analysis of Microarrays (SAM) method. Using this approach, 919 genes were identified that were significantly altered with rapid stimulation (763 up-regulated and 156 down-regulated). For many individual transcripts, changes typical of AF/AT were observed, with marked up-regulation of genes encoding BNP and ANP precursors, heat shock proteins, and MAP kinases, while novel signaling pathways and molecules were also identified. Both stress and survival response were evident, as well as up-regulation of multiple transcription factors. Genes were also functionally classified based on cellular component, biologic process, and molecular function using the Gene Ontology database to permit direct comparison of our data with other gene sets regulated in human AF and experimental AT. For broad categories of genes grouped by functional classification, there was striking conservation between rapidly stimulated HL-1 cells and AF/AT. Results were confirmed using real-time quantitative RT-PCR on 13 genes selected by physiological relevance in AF/AT and regulation in the microarray analysis (up, down, and nonregulated). Rapidly-stimulated atrial myocytes provide a complementary experimental paradigm to explore the initial cellular signals in AT remodeling to identify novel targets in the treatment of AF.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-10598

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28515
Effect of acute ethanol on medidal prefrontal cortex across BXD genetic mapping panel and progenitors.
  • organism-icon Mus musculus
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon

Description

In order to elucidate the molecular mechanisms underlying individual variation in sensitivity to ethanol we profiled the prefrontal cortex transcriptomes of two inbred strains that exhibit divergent responses to acute ethanol, the C57BL6/J (B6) and DBA/2J (D2) strains, as well as 27 members of the BXD recombinant inbred panel, which was derived from a B6 x D2 cross. With this dataset we were able to identify several gene co-expression networks that were robustly altered by acute ethanol across the BXD panel. These ethanol-responsive gene-enriched networks were heavily populated by genes regulating synaptic transmission and neuroplasticity, and showed strong genetic linkage to discreet chromosomal loci. Network-based measurements of node importance identified several hub genes as established regulators of ethanol response phenotypes, while other hubs represent novel candidate modulators of ethanol responses.

Publication Title

Genetic dissection of acute ethanol responsive gene networks in prefrontal cortex: functional and mechanistic implications.

Alternate Accession IDs

E-GEOD-28515

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE81468
Association of dysfunctional synapse defective 1 (SYDE1) with restricted fetal growth SYDE1 regulates placental cell migration and invasion
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

In this study, we identify SYDE1 as a novel GCM1 target gene. We demonstrate that SYDE1 promotes placental cell migration and invasion and that the GCM1-SYDE1 axis is crucial for placental development. Importantly, retarded placental and fetal growth with defective spongiotrophoblast layer, compromised vasculogenesis, and abnormal maternal-trophoblast interface are noted in the Syde1 homozygous knockout (KO) placenta. Along this line, decreased SYDE1 expression is observed in human IUGR placentas. We further demonstrated that components of the renin-angiotensin system (RAS) and Syde2 are differentially expressed in Syde1-KO placenta, which might contribute to normal neonatal delivery in Syde1-KO mothers

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-81468

Sample Metadata Fields

Specimen part

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accession-icon GSE50225
Wild-type and Mecp2 -/y callosal projection neurons
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Mutations of the transcriptional regulator Mecp2 cause the X-linked autism spectrum disorder Rett syndrome (RTT), and Mecp2 has been implicated in several other neurodevelopmental disorders. To identify potential target genes regulated directly or indirectly by MeCP2, we performed comparative gene expression analysis via oligonucleotide microarrays on Mecp2-/y (Mecp2-null) and wild-type CPN purified via fluorescence-activated cell sorting (FACS).

Publication Title

Reduction of aberrant NF-κB signalling ameliorates Rett syndrome phenotypes in Mecp2-null mice.

Alternate Accession IDs

E-GEOD-50225

Sample Metadata Fields

Specimen part

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accession-icon GSE17745
Identification of genes regulated by the RANK IVVY motif in macrophages
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Identification of genes regulated by RANK RVVY motif in macrophages by gene expression analysis of TNFR1-/-R2-/- BMMs expressing a chimeric receptor consisting of the external domain of mouse TNFR1 linked to the transmembrane and intracellular domain of mouse RANK (WT) and NFR1-/-R2-/- BMMs expressing a chimeric receptor consisting of the external domain of mouse TNFR1 linked to the transmembrane and intracellular domain of mouse RANK bearing inactivating mutations in the IVVY motif (Mu).

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-17745

Sample Metadata Fields

Specimen part

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accession-icon GSE30160
The RANK IVVY Motif-regulated Genes in Osteoclastogenesis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

By carrying out a systematic structure/function study of the RANK cytoplasmic domain, we previously identified a specific 4-a.a. RANK motif (IVVY535-538) which plays a critical role in osteoclastogenesis by mediating commitment of macrophages to the osteoclast lineage. We have recently validated the role of this IVVY motif in osteoclastogenesis in vivo by generating knockin (KI) mice bearing inactivating mutations in the RANK IVVY motif. This microarray experiment was performed to determine whether the IVVY motif is involved in regulating gene expression in osteoclastogenesis.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-30160

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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