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accession-icon GSE45916
Expression data from mouse embryonic fibroblasts and pluripotent stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Splicing profiles in pluripotent stem cells are different from those in somatic cells. Generally, alternative splicing is regulated by RNA binding proteins. To identify the candidate RNA-binding protein-encoding genes, we performed gene expression profiling experiments.

Publication Title

Global splicing pattern reversion during somatic cell reprogramming.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE90141
Gene expression analysis of human dermal fibroblasts (HDF) and human iPSC
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify the genes whose expression levels are changed before and after somatic cell reprogramming, we performed global gene expression analysis of iPS cells and their original fibrobrasts.

Publication Title

Structural and spatial chromatin features at developmental gene loci in human pluripotent stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE65468
Analysis of Klf4 factor stoichiometry effects during iPS cell derivation from mouse embryonic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Oct3/4, Sox2, Klf4, and c-Myc re-wire somatic cells to achieve induced pluripotency (iPS cells). However, subtle differences in reprogramming methodology may confound comparative studies of reprogramming-induced gene expression changes. We specifically focused on the design of polycistronic reprogramming constructs, which encode all four factors linked with 2A peptides. Notably, publically available cassettes were found to employ one of two Klf4 variants (Klf4S and Klf4L; GenBank Accession Nos: AAC52939.1 and AAC04892.1), differing only by nine N-terminal amino acids. In a polycistronic context, these two variants generated dissimilar protein stoichiometry, where Klf4L vectors produced more Klf4 protein than those encoding Klf4S.

Publication Title

KLF4 N-terminal variance modulates induced reprogramming to pluripotency.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE89079
Gene expression analysis of mouse embryonic fibroblasts reprogrammed with OSK, Esrrb and Zic3
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We report that Zic family (Zic1/2/3) and orphan nuclear receptors family (Esrrb and Nr5a2) transcription factors (TFs) synergistically enhance the reprogramming efficiency when transduced with Oct4, Sox2 and Klf4 (OSK) into murine fibroblasts. To identify the molecular mechanisms underlying this synergy, we analyzed global gene expression at 6 days after introduction of reprogramming factors. As a result, we found that primary targets of these TFs are different when either of TFs was introduced with OSK, but a significant portion of genes including pluripotency makers such as Dppa2 was synergistically upregulated. Further analysis revealed that metabolic pathways are the important targets of these TFs for efficient reprogramming.

Publication Title

Hybrid Cellular Metabolism Coordinated by Zic3 and Esrrb Synergistically Enhances Induction of Naive Pluripotency.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE52304
Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Premature termination of reprogramming in vivo leads to cancer development through altered epigenetic regulation.

Sample Metadata Fields

Specimen part

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accession-icon GSE51786
Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We report a reprogrammable mouse system in which reprogramming factor expression in vivo can be controlled temporally by treatment with doxycycline (Dox). Transient expression of reprogramming factors in vivo results in tumor development in various tissues, consisting of undifferentiated dysplastic cells. We analyzed the kidney tumors developed in reprogrammable mice for global gene expressions and DNA methylations.

Publication Title

Premature termination of reprogramming in vivo leads to cancer development through altered epigenetic regulation.

Sample Metadata Fields

Specimen part

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accession-icon GSE99316
Gene repression and ChIP-seq in Human Small Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PRC2 overexpression and PRC2-target gene repression relating to poorer prognosis in small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE43346
Gene repression with H3K27me3 modification in human small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Small cell lung cancer (SCLC) is a subtype of lung cancer with poor prognosis due to early dissemination and rapid growth. We here analyze gene expression profile of 23 clinical SCLC samples. EZH2 was found to be highly expressed in SCLC samples compared to 42 normal tissues including the normal lung, and other PRC2 members, SUZ12 and EED, were also highly expressed in SCLC. To obtain target genes of PRC2 in SCLC, H3K27me3 mark was mapped in three SCLC cell lines, Lu130, H209 and DMS53, and compared to normal small airway epithelial cells (SAEC). Whereas H3K27me3(+) genes in SAEC were significantly overlapped with PRC-target genes in ES cells (P=1.7x10-31), genes with H3K27me3 in SCLC cell lines but not in SAEC were not significantly overlapped with PRC-target genes in ES cells (P=0.64). These genes with H3K27me3 specifically in SCLC cell lines but not in SAEC showed decreased expression, not only in SCLC cell lines but also in clinical SCLCs, and showed enrichment of GO-terms such as plasma membrane (P=8.1x10-21) and cell adhesion (P=1.7x10-8). Introduction of JUB, a gene showing specific H3K27me3 modification and the strongest repression in the three SCLC cell lines, resulted in repression of cellular growth in DMS53. In clinical SCLC cases, lower JUB level correlated to shorter survival (P=0.002), or a set of PRC target genes (JUB, EPHB4) and marker genes of classic type SCLC (GRP, ASCL1) correlated to shorter survival (P=0.0001) and classified SCLC into two groups with distinct prognosis. Growth of SCLC cell lines was repressed when treated with 3-Deazaneplanocin A, an inhibitor against PRC2. It is suggested that high expression of PRC2 in SCLC contributed to repression of genes including non-PRC-target genes in ES cells, and that the gene repression may play a role in genesis of SCLC.

Publication Title

PRC2 overexpression and PRC2-target gene repression relating to poorer prognosis in small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE11128
Expression data from single cells from mouse primordial germ cell lineage (E6.25-E8.25, wild type and Blimp1KO)
  • organism-icon Mus musculus
  • sample-icon 105 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Specification of germ cell fate is fundamental in development. With a highly representative single-cell microarray and rigorous quantitative-PCR analysis, we defined the genome-wide transcription dynamics that create primordial germ cells (PGCs) from the epiblast, a process that exclusively segregates them from their somatic neighbors. We also analyzed the effect of the loss of Blimp1, a key transcriptional regulator, on these dynamics. Our analysis revealed that PGC specification involves complex, yet highly ordered regulation of a large number of genes, proceeding under the strong influence of mesoderm induction with active repression of specific programs such as epithelial-mesenchymal transition, Hox gene activation, cell-cycle progression and DNA methyltransferase machinery. Remarkably, Blimp1 is essential for repressing nearly all the genes normally down-regulated in PGCs relative to their somatic neighbors, whereas it is dispensable for the activation of approximately half of the genes up-regulated in PGCs.

Publication Title

Complex genome-wide transcription dynamics orchestrated by Blimp1 for the specification of the germ cell lineage in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE34000
Expression data from the dorsal root ganglia during streptozotocin-induced painful diabetic neuropathy in rats
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

FK1706 potentiated nerve growth factor-induced neurite outgrowth, putatively mediated via FKBP-52 and the Ras/Raf/MAPK signaling pathway. It also improved mechanical allodynia accompanied by the recovery of intraepidermal nerve fiber density in a painful diabetic neuropathy in rats.

Publication Title

FK1706, a novel non-immunosuppressive immunophilin ligand, modifies gene expression in the dorsal root ganglia during painful diabetic neuropathy.

Sample Metadata Fields

Specimen part, Treatment

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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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