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accession-icon GSE3542
Profiling of MCF-7 cell lines stably overexpressing (ca)Raf-1, (ca)MEK, (ca)erbB-2, or ligand-activatable EGFR.
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1, constitutively active MEK, constitutively active c-erbB-2, or ligand-activatable EGFR as models of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2).

Publication Title

Activation of mitogen-activated protein kinase in estrogen receptor alpha-positive breast cancer cells in vitro induces an in vivo molecular phenotype of estrogen receptor alpha-negative human breast tumors.

Sample Metadata Fields

Cell line

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accession-icon GSE29004
Gene expression response to acrylamide in rat pups
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Acrylamide is a type-2 alkene monomer with established human neurotoxic effects. While the primary source of human exposure to acrylamide is occupational, other exposure sources include food, drinking water, and smoking. In this study, neurobehavioral assays coupled with transcriptional profiling analysis were conducted to assess both behavioral and gene expression effects induced by acrylamide neurotoxicity in rats when administered during early postnatal life. Acrylamide administration in rat pups induced significant characteristic neurotoxic symptoms including increased heel splay, decrease in grip strength, and decrease in locomotor activity. Transcriptome analysis with the Affymetrix Rat Genome 230 2.0 array indicated that acrylamide treatment caused a significant alteration in the expression of genes involved in muscle contraction, pain regulation, and dopaminergic neuronal pathways. First, in agreement with the observed behavioral effects, expression of the Mylpf gene involved in muscle contraction was downregulated in the spinal cord in response to acrylamide. Second, in sciatic nerves, acrylamide repressed the expression of the opioid receptor gene Oprk1 that is known to play a role in neuropathic pain regulation. Finally, in the cerebellum, acrylamide treatment caused a decrease in the expression of the nuclear receptor gene Nr4a2 that is required for development of dopaminergic neurons. Thus, our work examining the effect of acrylamide at the whole-genome level on a developmental mammalian model has identified novel genes previously not implicated in acrylamide neurotoxicity that can be further developed into biomarkers for assessing the risk of acrylamide exposure.

Publication Title

Neurobehavioral and transcriptional effects of acrylamide in juvenile rats.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP071547
Dynamic gene regulatory networks of human myeloid differentiation [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

We utilize gene expression and open chromatin footprinting data to build a gene regulatory network of key transcription factors that capture the cell and time-specific regulatory programs specified during human myeloid differentiation. Overall design: RNA-seq profiling of undifferentiated HL-60, differentiating macrophage, neutrophil, monocyte, and monocyte-derived macrophage cells.

Publication Title

Dynamic Gene Regulatory Networks of Human Myeloid Differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP092251
Integrative analysis of single-cell ATAC-seq and RNA-seq using Self-Organizing Maps [scRNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 568 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We have developed a computational approach that uses self-organizing maps for integrative genomic analysis. We utilize this approach to identify the single-cell chromatin and transcriptomic profiles during mouse pre-B cell differentiation. Overall design: We use the C1 Fluidigm system to profile gene expression and chromatin accessibility in single-cells during pre-B cell differentiation.

Publication Title

Building gene regulatory networks from scATAC-seq and scRNA-seq using Linked Self Organizing Maps.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP072875
Single-nucleus RNA-seq on undifferentiated human KD3 myoblasts and differentiated myotubes and mononucleated cells.
  • organism-icon Homo sapiens
  • sample-icon 253 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report the application of single-nucleus-based sequencing technology for high-throughput profiling of transcriptome in immortazalized human myoblast KD3. By obtaining over sixty billion bases of sequence from mRNA, we generated comprehensive transcriptome profiles from KD3 undifferentiated myoblast and differentiated multi-nucleated myotube and mono-nucleated cells. We find that the data from single-nucleus RNA-seq is consistent with the transcriptome from single-cell RNA-seq. The pri-mRNA expression characterized by single-nucleus RNA-seq can reflect the actual miRNA level in the whole cell. Overall design: Examination of transcriptome in 1 cell type in 3 differential stages.

Publication Title

Single-nucleus RNA-seq of differentiating human myoblasts reveals the extent of fate heterogeneity.

Sample Metadata Fields

Subject

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accession-icon SRP073725
Chd5 regulates a ribosome biogenesis switch controlling neural cell fate specification
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Cell fate specification of neural stem/progenitor cells (NSCs) is an intricate developmental process that determines neural cell identity. While transcriptional mechanisms undoubtedly affect this process, translational mechanisms are much less understood. Here we show that deficiency of the chromatin remodeler Chromodomain Helicase DNA binding protein 5 (Chd5) causes transcriptional de-repression of multiple ribosomal subunit genes, increases protein synthesis, and expands the activated stem cell pool leading to perturbation of NSC fate. Compromised H3K27me3 in Chd5 deficient NSCs during early cell fate specification underlies the generation of excessive astrocytes at the expense of neurons at later stages of differentiation. Chd5 expression rescues these cell fate defects while simultaneously reestablishing H3K27me3, and inhibition of the H3K27me3-specific demethylase Utx restores appropriate cell fate specification in NSCs lacking Chd5. These findings define a Chd5-Utx-H3K27me3 axis pivotal in ribosome biogenesis and translation during neurogenesis, consistent with compromised CHD5 being implicated in glioma. Overall design: mRNA profiles of primary neural/stem progenitor cells (NSCs) of wild type (+/+) and Chd5-/- mice were generated, in duplicate, using Illumina NextSeq 500.

Publication Title

Chromatin-mediated translational control is essential for neural cell fate specification.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE102453
Endotoxin preconditioning reprograms S1 tubules and macrophages to protect the kidney
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Preconditioning with a small dose of endotoxin confers unparalleled protection against otherwise lethal models of sepsis. The mechanisms of preconditioning have been investigated extensively in isolated immune cells such as macrophages. However, the role of tissue in mediating the protective response to preconditioning remains unknown. Using the kidney as a model organ, we identify the essential role of the renal epithelial cell in mediating the full expression of protective preconditioning. The protective phenotype is characterized by the clustering of macrophages around S1 segments of proximal tubules, which forms a functional unit mediating protection. To investigate the molecular pathways, we laser microdissected S1 segments from the following: 1) Non-preconditioned mice subjected to single-dose 5 mg/kg lipopolysaccharide (0111:B4, LPS) intraperitoneally for 24 hours. 2) Preconditioned mice subjected to 0.25 mg/kg LPS followed 24 hour later by 5 mg/kg LPS (LPS/LPS). 3) Control mice (saline vehicle).

Publication Title

Endotoxin Preconditioning Reprograms S1 Tubules and Macrophages to Protect the Kidney.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE62834
Expression data from E15.5 mouse embryos
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The pancreatic beta cells are the only cells that can produce insulin in response to prevailing glycemia. The development of beta cells was found to be depending on the activity of a complex genetic network. Overexpression of transcriptional factor MafK in beta cells have resulted in impairment of thier functions and suppressed insulin secretion and increased the severity of beta cell loss resulting in an overt diabetes.

Publication Title

β-Cell-Specific Mafk Overexpression Impairs Pancreatic Endocrine Cell Development.

Sample Metadata Fields

Specimen part

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accession-icon GSE136219
Circulating Uromodulin inhibits systemic oxidative stress by inactivating the TRPM2 channel
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

High serum concentrations of kidney-derived protein uromodulin (Tamm-Horsfall protein or THP) have recently been shown to be independently associated with low mortality   in both older adults and cardiac patients, but the underlying mechanism remains unclear. Here, we show that THP inhibits the generation of reactive oxygen species (ROS) both in the kidney and systemically. Consistent with this experimental data, the concentration of circulating THP in patients with surgery-induced acute kidney injury (AKI) correlated with systemic oxidative damage. THP in the serum dropped after AKI, and was associated with an increase in systemic ROS. The increase in oxidant injury correlated with post-surgical mortality and need for dialysis. Mechanistically, THP inhibited the activation of the TRPM2 channel. Furthermore, inhibition of TRPM2 in vivo in a mouse model, mitigated the systemic increase in ROS during AKI and THP deficiency. Our results suggest that THP is a key regulator of systemic oxidative stress by suppressing TRPM2 activity and our findings might help to explain how circulating THP deficiency is linked with poor outcomes and increased mortality.

Publication Title

Circulating uromodulin inhibits systemic oxidative stress by inactivating the TRPM2 channel.

Sample Metadata Fields

Specimen part

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accession-icon SRP056404
High-throughput sequencing reveals key genes and immune homeostatic pathways activated in myeloid dendritic cells by Porphyromonas gingivalis 381 and its fimbrial mutants
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Periodontitis affects 47.1% of adult population in the U.S. Porphyromonas gingivalis is an opportunistic oral pathogen that colonizes the oral mucosa, invades myeloid dendritic cells and accesses the bloodstream, brain, placenta and other organs in human with periodontitis. Periodontitis also sustains a chronic long-term pro-inflammatory immune disorder, potentially contributing to other systemic conditions such as cardiovascular disease, type 2 diabetes mellitus, adverse pregnancy outcomes, and osteoporosis. However, the role of P. gingivalis minor and major fimbriae in DC-SIGN-TLR2 crosstalk during traverses from oral mucosa to these distant sites and its influence on survival of P. gingivalis within DCs and its immune-mechanism involve at molecular/transcriptome level has not been examined. In this study to address the role of fimbriae we utilized defined bacterial mutants that solely express minor fimbriae (Mfa1+Pg), major fimbriae (FimA+Pg) or are deficient in both fimbriae (MFB) and compared with un-infected control. P. gingivalis strains were maintained anaerobically (10% H2, 10% CO2, and 80% N2) in a Forma Scientific anaerobic system glove box model 1025/1029 at 37°C in Difco anaerobe broth MIC. Mutant strains were maintained using erythromycin (5 µg/ml) for mutant Mfa1+Pg, tetracycline (2 µg/ml) for mutant FimA+Pg and both erythromycin and tetracycline for double fimbriae mutant MFB. Bacterial suspensions were washed five times in PBS and re-suspended for spectrophotometer reading at OD 660 nm of 0.11, which previously determined to be equal to 5 x 107 CFU. For bacterial CFSE staining, the suspension were washed (3 times) and re-suspended in 5 µM of CFSE in PBS. The bacteria were incubated for 30 min at 37°C in the dark. MoDCs were pulsed with Pg381, Mfa1+Pg, FimA+Pg and MFB at 10 MOI and incubated with the MoDCs for 12 hours and each experimental condition was performed in triplicate. Overall design: To facilitate our understanding on host immunity and defense mechanism of this pathogen, here we used the Illumina High-throughput RNA-seq transcriptome profiling to investigate the myeloid dendritic cells response to oral Amphibiont (1. Pg381, 2. Mfa1+Pg, 3. FimA+Pg, 4. MFB and 5. Un-infected control group).

Publication Title

Oral Pathobiont Activates Anti-Apoptotic Pathway, Promoting both Immune Suppression and Oncogenic Cell Proliferation.

Sample Metadata Fields

No sample metadata fields

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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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