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accession-icon GSE136895
Plant toxin treatment of neonatal mouse cholangiocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Extrahepatic bile ducts were isolated from mouse pups at days 0-3 and primary cholangiocytes were isolated. Cholangiocytes were treated with DMSO, bilatresone (TOX4), betavulgarin (TOX2), and isoflavanone (TOX3), as per Lorent et al, Science Translationa Medicine 2015;286:286ra67 (Fig. 1), all in DMSO. Treatment concentrations were 2.0 micrograms/ml, for 6 hours.

Publication Title

Extrahepatic cholangiocyte obstruction is mediated by decreased glutathione, Wnt and Notch signaling pathways in a toxic model of biliary atresia.

Sample Metadata Fields

Treatment

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accession-icon SRP068364
Transcriptional profiling through RNA-seq of zebrafish larval liver after exposure to biliatresone, a biliary toxin.
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We sequenced liver mRNA isolated from biliatresone-treated zebrafish larvae and DMSO-treated controls in order to elucidate the molecular pathways induced by biliatresone, a biliary toxin that is responsible for outbreaks of biliary atresia in Australian liverstock. Overall design: Liver mRNA profiles of biliatresone-treated zebrafish larvae and DMSO-treated controls were generated by deep sequencing, in duplicates.

Publication Title

Glutathione antioxidant pathway activity and reserve determine toxicity and specificity of the biliary toxin biliatresone in zebrafish.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54219
Molecular genomic and transcriptomic profiling of familial breast cancer.
  • organism-icon Homo sapiens
  • sample-icon 155 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genomic profiling of CHEK2*1100delC-mutated breast carcinomas.

Sample Metadata Fields

Specimen part

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accession-icon SRP067537
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

One of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner. Overall design: Sorted splenic dendritic cell subsets from either Flt3+/+ or Flt3ITD/+ mice were sequenced for mRNA profiling. For each subset per genotype contains 2-3 replicates, all from independent experiments.

Publication Title

Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP159271
Innate mesenchymal TLR4/MyD88 signals promote spontaneous intestinal tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

This study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model. Overall design: 3' RNA-Seq (QuantSeq) profiling of ColVIcre+ wt and MyD88 knockout primary mouse intestinal mesenchymal cells before and after treatment with LPS for 6 hours. 3 replicates per group.

Publication Title

Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE111450
Expression data from murine colorectal tumours of control and IL-6Ralpha-deficient mice fed a high fat diet
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Obesity increases colorectal cancer despite other disturbances. We have used the AOM/DSS protocol to induce colitis-associated cancer in control and IL-6Ra deficient animals. Tumours were microdissected and globalgene expression was analysed using microarray.

Publication Title

Obesity exacerbates colitis-associated cancer via IL-6-regulated macrophage polarisation and CCL-20/CCR-6-mediated lymphocyte recruitment.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP071039
Novel neuroprotective and neurogenic phenotype of microglia
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Background: Tissue macrophages contribute to development and protection, both requiring appropriately timed and located source(s) of factors controlling growth, cell differentiation and migration. Goal: To understand the role of microglia (tissue macrophages of the central nervous system), in promoting neurodevelopment and controlling neuroinflammation. Summary of findings: We show that microglia fulfill both these roles. In contrast to adult cells, neonatal microglia show a unique neurogenic phenotype with stem cell-like potential. Neonatal microglia are protective against neuroinflammation, and their transplantation ameliorates experimental autoimmune encephalomyelitis. A CD11c+ microglial subset predominates in primary myelinating areas of the developing brain and expresses genes for neuronal and glial survival, migration and differentiation. CD11c+ microglia are also found in clusters of repopulating microglia after experimental ablation and in neuroinflammation in adult mice, but despite some similarities, they do not recapitulate neurogenic neonatal microglia characteristics. Conclusions: We therefore identify a unique phenotype of neonatal microglia that deliver signals necessary for neurogenesis and myelination and suppress neuroinflammation. Overall design: The overall design was to compare transcriptomes of subsets of microglia isolated from neonatal mice, healthy adults, and adult mice with a neuroinflammatory disease (Experimental autoimmune encephalomyelitis, EAE), and to compare anti-inflammatory function of adult and neonatal microglia. Microglia were isolated by cell-sorting based on surface phenotype, and RNAseq data was analyzed using WGCNA, GO and DAVID approaches. Expression of selected genes and pathways was confirmed by histology and flow cytometry. Functional analysis involved transfer of isolated microglia to the central nervous system of animals with EAE and evaluation of outcome. EAE = Experimental autoimmune encephalomyelitis

Publication Title

A novel microglial subset plays a key role in myelinogenesis in developing brain.

Sample Metadata Fields

Subject

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accession-icon SRP043035
IL-17A induces inhibition of OB function
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We report that IL-17A has an inhibitory effect on osteoblastogenesis. Overall design: Pre-osteoblasts were treated with vehicle or 50ng/ml IL-17A for 7 days.

Publication Title

Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32209
Tumor-Derived G-CSF Facilitates Neoplastic Growth through a Granulocytic Myeloid-Derived Suppressor Cell-Dependent Mechanism
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Global gene expression studies were performed to determine whether the granulocytic-like MDSC populations from G-CSF treated mice resembled those of tumor-bearing (TB) mice more so than those of the non-tumor-bearing control (i.e., WT) at a molecular level.

Publication Title

Tumor-derived G-CSF facilitates neoplastic growth through a granulocytic myeloid-derived suppressor cell-dependent mechanism.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE65721
RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.

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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