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accession-icon GSE91374
A Molecular Roadmap for Induced Multi-lineage Trans-differentiation of Fibroblasts by Chemical Combinations
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A molecular roadmap for induced multi-lineage trans-differentiation of fibroblasts by chemical combinations.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE91005
A Molecular Roadmap for Induced Multi-lineage Trans-differentiation of Fibroblasts by Chemical Combinations [gene expression]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Recent advances highlight the power of small molecules for promoting cellular reprogramming. Yet, the full potential of such chemicals in cell fate manipulation and the underlying mechanisms needs further characterization. Through functional screening assays, we found that mouse embryonic fibroblast can be induced to trans-differentiate into a wide range of somatic lineages simultaneously by treatment with a combination of four chemicals. Genomic analysis of the process indicates activation of multi-lineage modules and relaxation of epigenetic silencing programs. In addition, we identify Sox2 as an important regulator within the induced network. Single cell analysis uncovers a priming state that enables transition from fibroblast cells to diverse somatic lineages. Finally, we demonstrate that modification of the culture system enables directional trans-differentiation towards cardiac, neuronal or adipocytic lineages. Our study describes a cell fate control system that may be harnessed for regenerative medicine.

Publication Title

A molecular roadmap for induced multi-lineage trans-differentiation of fibroblasts by chemical combinations.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon SRP056597
High-fat diet enhances stemness and tumorigenicity of intestinal progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. Overall design: mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.

Publication Title

High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP151504
Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Renal artery stenosis (RAS) caused by narrowing of arteries is characterized by microvascular damage. Macrophages are implicated in repair and injury, but the specific populations responsible for these divergent roles have not been identified. Here, we characterized murine kidney F4/80+CD64+ macrophages in three transcriptionally unique populations. Using fate-mapping and parabiosis studies, we demonstrate that CD11b/cint are long-lived kidney-resident (KRM) while CD11chiMf, CD11cloMf are monocyte-derived macrophages. In a murine model of RAS, KRM self-renewed, while CD11chiMf and CD11cloMf increased significantly, which was associated with loss of peritubular capillaries. Replacing the native KRM with monocyte-derived KRM using bone marrow transplantation followed by RAS, amplified loss of peritubular capillaries. To further elucidate the nature of interactions between KRM and peritubular endothelial cells, we performed RNA-sequencing on flow-sorted macrophages from Sham and RAS kidneys. KRM showed a prominent activation pattern in RAS with significant enrichment in reparative pathways, like angiogenesis and wound healing. In culture, KRM increased proliferation of renal peritubular endothelial cells implying direct pro-angiogenic properties. Human homologs of KRM identified as CD11bintCD11cintCD68+ increased in post-stenotic kidney biopsies from RAS patients compared to healthy human kidneys, and inversely correlated to kidney function. Thus, KRM may play protective roles in stenotic kidney injury through expansion and upregulation of pro-angiogenic pathways Overall design: CD11chiMf Sham, n=3; CD11chiMf RAS, n=4; CD11cloMf Sham, n=3; CD11cloMf RAS, n=4; KRM Sham, n=4; KRM RAS, n=3;

Publication Title

Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon GSE56251
Expression data from Escherichia coli after treatment with nalidixic acid (NA)
  • organism-icon Escherichia coli
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Having found that LexA degradation was significantly higher under apoptotic like death (ALD) than under SOS conditions, we hypothesized that additional genes tightly regulated by LexA would be transcribed under ALD conditions.

Publication Title

Apoptosis-like death, an extreme SOS response in Escherichia coli.

Sample Metadata Fields

Disease, Treatment

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accession-icon SRP064569
Effect of LSD1 depletion on gene expression in oocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The objective of the experiment is to compare the transcriptomes of LSD1 knockout (KO) and control oocytes Overall design: RNA-seq analysis of GV oocytes, with three biological replicates for each genotype

Publication Title

Dynamic changes in histone modifications precede de novo DNA methylation in oocytes.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP073613
Identification of mRNAs with reduced ribosomal loading upon knock-down of translation factor DAP5 from hESCs.
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We have generated stable human ESCs (H9) expressing control or DAP5-targeting shRNA. Polysome profiles reveal no major changes in overall translation. PolyA+ RNA and RNA accociated with heavy polysomal fractions were purified in biological duplicates and sequenced using Illumina HiSeq 2000 instrument. We identified 122 potential mRNA targets of DAP5 translation that display reduced ribosomal loading, and hence reduced translation, in the absence of DAP5. Overall design: Total mRNA and heavy polylsomal fractions from shNT and shDAP5 expressing hESCs, each in duplicate, was deep sequenced.

Publication Title

Cap-independent translation by DAP5 controls cell fate decisions in human embryonic stem cells.

Sample Metadata Fields

Subject

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accession-icon SRP028118
Derivation of endothelial colony forming cells from human pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Human induced pluripotent stem (hiPS) cells and human embryonic stem (hES) cells differentiate into cells of the endothelial lineage, but derivation of cells with human umbilical cord blood endothelial colony forming cell (ECFC)-like properties has not been reported. Here we describe a novel serum- and stromal cell-free ECFC differentiation protocol for the derivation of clinically relevant numbers of ECFCs (> 108) from hiPS and hES cells. We identified NRP-1+CD31+ selected cells that displayed a stable endothelial phenotype exhibiting high clonal proliferative potential, extensive replicative capacity, formation of human vessels that inosculated with host vasculature upon transplantation, but lacking in teratoma formation in vivo. We also identified NRP-1-VEGF165-KDR-mediated activation of KDR as a critical mechanism for the emergence and derivation of ECFCs from hiPS and hES cells. This protocol advances the field by generating highly replicative but stable endothelial cells for use as a potential cell therapy for human clinical disorders. Overall design: Transcriptome sequencing of undifferentiated day 0 hiPS cells, Day 3 differentiated hiPS-derived mesoderm proginator cells, Day 12 hiPS-derived NRP-1+CD31+ cells, Day 12 H9-hES-derived NRP-1+CD31+ cells and cord blood-derived Endothelial colony forming cells.

Publication Title

Differentiation of human pluripotent stem cells to cells similar to cord-blood endothelial colony-forming cells.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE42834
Human whole blood microarray study to compare patients with tuberculosis, sarcoidosis, pneumonia, and lung cancer
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional blood signatures distinguish pulmonary tuberculosis, pulmonary sarcoidosis, pneumonias and lung cancers.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment, Race, Subject

View Samples
accession-icon GSE42830
Human whole blood microarray study to compare patients with tuberculosis, sarcoidosis, pneumonia, and lung cancer (training)
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This study used whole blood transcriptional signatures from patients with tuberculosis compared to those with similar pulmonary diseases, sarcoidosis, pneumonia and primary lung cancer. TB and sarcoidosis had similar signatures that were distinct from pneumonia and lung cancer.

Publication Title

Transcriptional blood signatures distinguish pulmonary tuberculosis, pulmonary sarcoidosis, pneumonias and lung cancers.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Race

View Samples
...

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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