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accession-icon GSE97396
Lamin A/C ablation in pancreatic acinar cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Lamin A/C was ablated in pancreatic acinar cells using Elastase1 driven, Cre-ErT mediated, LoxP recombination, causing excision of exons 10 and 11 of the Lmna gene

Publication Title

Lamin A/C Maintains Exocrine Pancreas Homeostasis by Regulating Stability of RB and Activity of E2F.

Sample Metadata Fields

Sex

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accession-icon GSE96820
Gene expression altered by high-fructose diet feeding and Chrebp deficiency
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Epidemiologic and animal studies implicate overconsumption of fructose in the development of non-alcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remains largely unknown. We present evidence supporting the essential function of the lipogenic transcription factor ChREBP in mediating adaptation response to fructose and protecting against fructose-induced hepatotoxicity. High-fructose diet (HFrD) activates hepatic lipogenesis via a ChREBP-dependent manner in wildtype mice, while inducing steatohepatitis in Chrebp-KO mice. In Chrebp-KO mouse livers, HFrD reduces levels of molecular chaperones and activates the CHOP-dependent unfolded protein response, whereas administration of chemical chaperone or Chop shRNA rescues liver injury. Gene expression profiling revealed elevated expression of cholesterol biosynthesis genes in Chrebp-KO livers after HFrD, in parallel with increased abundance of nuclear SREBP2.

Publication Title

Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE12989
Foxl2 functions throughout mouse ovary development
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Foxl2 functions in sex determination and histogenesis throughout mouse ovary development.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE12905
Foxl2 functions in sex determination and histogenesis throughout mouse ovary development, analyzed by Affymetrix arrays
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development.

Publication Title

Foxl2 functions in sex determination and histogenesis throughout mouse ovary development.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-2127
Transcription profiling of yeast grown in gastric or duodenal medium to identify promoters that could be used to down-regulate genes used in the release of therapeutic proteins
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The use of yeast as a delivery system is an attractive option for the oral administration of therapeutic agents. We recently developed mutants of Saccharomyces cerevisiae capable of lysis upon conditional down-regulation of the expression of the cell wall genes PKC1 and SRB1. The lysis mechanism of the mutant is based on the use of the MET3 promoter, which, upon addition of methionine and cysteine, blocks transcription of SRB1 and PKC1. This strain has the potential to be an integral part of an oral yeast delivery system, in which there is lysis of yeasts in the human gut, followed by release of recombinant proteins for therapeutic use. In order to provide proof-of-principle, the system was evaluated testing the cells viability and lysis performance under conditions, which simulate those found in the human stomach and the duodenum. Upon incubation of yeast cells in these conditions, lysis could be induced and was accompanied by release of GFP reporter protein into the medium. However, the conditional lysis mechanism based on the MET3 promoter is not applicable in vivo. Therefore, alternative promoters suitable for in-vivo down-regulation of SRB1 and PKC1 were identified by a microarray experiments. The transcripts of genes ANB1, TIR1, and MF(ALPHA)2 were significantly reduced upon exposure of the yeast cells to conditions of the two gut compartments. Their promoters could be used to down-regulate SRB1/VIG9 and PKC1 in vivo to achieve lysis of the yeast in the gut to release cargo therapeutic proteins.

Publication Title

Conditional cell-wall mutants of Saccharomyces cerevisiae as delivery vehicles for therapeutic agents in vivo to the GI tract.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49231
Clonal Genetic and Hematopoietic Heterogeneity among Human Induced Pluripotent Stem Cell lines
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Induced pluripotent stem cells hold great promise for modeling human hematopoietic diseases. However, intrinsic variability in the capacities of different iPSC lines for hematopoietic development complicates comparative studies and is currently unexplained.

Publication Title

Clonal genetic and hematopoietic heterogeneity among human-induced pluripotent stem cell lines.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE61421
PARP9 and DTX3L in Antiviral Host Defense
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon (lluminamouse6v1.1expressionbeadchip[arrayaddressidversion), Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PARP9-DTX3L ubiquitin ligase targets host histone H2BJ and viral 3C protease to enhance interferon signaling and control viral infection.

Sample Metadata Fields

Sex, Cell line, Treatment

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accession-icon GSE61413
Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon (lluminamouse6v1.1expressionbeadchip[arrayaddressidversion)

Description

U3A cells stably expressing wild-type STAT1 or STAT1-CC were treated with interferon beta (10U/ml) or control for 24 hours to assess effects of stat1 modifications, interferon, and the interaction on gene expression.

Publication Title

PARP9-DTX3L ubiquitin ligase targets host histone H2BJ and viral 3C protease to enhance interferon signaling and control viral infection.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP155569
RNA-seq of Single-Cell Genotyping of Transcriptomes
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Somatic cancer driver mutations may result in distinctly diverging phenotypic outputs. Thus, a common driver lesion may result in cancer subtypes with distinct clinical presentations and outcomes. The diverging phenotypic outputs of mutations result from the superimposition of the mutations with distinct progenitor cell populations that have differing lineage potential. However, our ability to test this hypothesis has been challenged by currently available tools. For example, flow cytometry is limited in its inability to resolve lineage commitment of early progenitors. Single-cell RNA sequencing (scRNA-seq) may provide higher resolution mapping of the early progenitor populations as long as high throughput technology is available to sequence thousands of single cells. Nevertheless, high throughput scRNA-seq is limited in its inability to jointly and robustly detect the mutational status and the transcriptional profile from the same cell. To overcome these limitations, we propose the use of scRNA-seq combined with targeted mutation sequencing from transcrptional read-outs. Overall design: We apply this method to study myeloid neopasms, in which the comlex process of hematopoiesis is corrupted by mutated stem and progenitor cells.

Publication Title

Somatic mutations and cell identity linked by Genotyping of Transcriptomes.

Sample Metadata Fields

Sex, Age, Disease, Treatment, Subject

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accession-icon GSE58037
Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO.
  • organism-icon Homo sapiens
  • sample-icon 114 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We report genomic analysis of 300 meningiomas, the most common primary brain tumors, leading to the discovery of mutations in TRAF7, a proapoptotic E3 ubiquitin ligase, in nearly one-fourth of all meningiomas. Mutations in TRAF7 commonly occurred with a recurrent mutation (K409Q) in KLF4, a transcription factor known for its role in inducing pluripotency, or with AKT1(E17K), a mutation known to activate the PI3K pathway. SMO mutations, which activate Hedgehog signaling, were identified in ~5% of non-NF2 mutant meningiomas. These non-NF2 meningiomas were clinically distinctive-nearly always benign, with chromosomal stability, and originating from the medial skull base. In contrast, meningiomas with mutant NF2 and/or chromosome 22 loss were more likely to be atypical, showing genomic instability, and localizing to the cerebral and cerebellar hemispheres. Collectively, these findings identify distinct meningioma subtypes, suggesting avenues for targeted therapeutics.

Publication Title

Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO.

Sample Metadata Fields

Disease stage

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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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