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accession-icon GSE26575
Human Induced Pluripotent Stem Cells Harbor Homoplasmic and Heteroplasmic Mitochondrial DNA Mutations While Maintaining human embryonic stem cells-like Metabolic Reprogramming
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Gene expression analyis of two hESCs, two human neonatal fibroblasts, and four human iPSCs generated with retroviral transduction using the OSKM cocktail.

Publication Title

Human induced pluripotent stem cells harbor homoplasmic and heteroplasmic mitochondrial DNA mutations while maintaining human embryonic stem cell-like metabolic reprogramming.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP165224
Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The gene regulatory network in naïve mouse embryonic stem cells (ESCs) must be reconfigured for lineage competence. Tcf3 enables rewiring to formative pluripotency by repressing components of the ESC transcription factor circuitry. However, elimination of Tcf3 only delays, and does not prevent, state transition. Here we delineate distinct contributions of the Ets-family transcription factor Etv5 and the repressor Rbpj. Downstream of Erk1/2 signalling, Etv5 activates enhancers for formative pluripotency. Concomitant up-regulation of Rbpj ensures irreversible exit from the naïve state by extinguishing reversal factors, Nanog and Tbx3. Triple deletion of Etv5, Rbpj and Tcf3 incapacitates ESCs, such that they remain undifferentiated and locked in self-renewal even in the presence of differentiation stimuli. Thus, pluripotency progression is driven hierarchically by two repressors, that respectively dissolve and extinguish the naive network, and an initiator that commissions the formative network. Similar tripartite action may be a general mechanism for efficient cell transitions. Overall design: RNA-seq analysis of parental Rex1-GFPd2 ES cells (RGd2), and deletion mutants generated in this background (Etv5-KO, RbpJ-KO, Etv5-RpbJ-dKO, Etv5-RbpJ-Tcf3-tKO) cultured in 2i, N2B27 or supplemented with Chiron, 3 biological replicates per condition.

Publication Title

Complementary Activity of ETV5, RBPJ, and TCF3 Drives Formative Transition from Naive Pluripotency.

Sample Metadata Fields

Subject

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accession-icon GSE37709
HIF1alpha drives early induction of pluripotency through reprogramming of glycolytic metabolism
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Gene expression analyis of two neonatal fibroblasts (BJ and HFF1), one adult dermal fibroblasts (NFH2), two BJ-derived human iPSCs (iB4 and iB5), two HFF1-derived iPSCs (iPS 2 and iPS4), four NFH2-derived iPSCs (OiPS3, OiPS6, OiPS8, OiPS16), one amniotic fluid cells and three derived iPSCs (lines 4, 5, 6, 10, and 41), two human ES cells (H1 and H9), neonatal fibroblasts transduced with the four retroviral factors (OKSM) after 24h, 48h, and 72h, neonatal fibroblasts treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts transduced with four factors and treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts knocked down for HIF1A (HIF1-KD) and for a scrambled sequence (SCR-KD)

Publication Title

HIF1α modulates cell fate reprogramming through early glycolytic shift and upregulation of PDK1-3 and PKM2.

Sample Metadata Fields

Age, Specimen part, Cell line

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accession-icon GSE15519
Expression and ChIP-seq analyses of embryonic stem cells, extraembryonic endoderm stem cells, and trophoblast stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Bivalent histone domains have been proposed to contribute to pluripotency in embryonic stem cells, suggesting an epigenetic mechanism may regulate stem cell behavior in general. Here we compare histone modifications in two other stem cells derived from the blastocyst. We show that extraembryonic stem cells have little repressive lysine 27 trimethylation and few bivalent domains. Thus, bivalent domains are not a common mechanism for maintaining the undifferentiated state in blastocyst-derived stem cells and alternative mechanisms must mediate transcriptional repression in extraembryonic cells. We show that lysine 9 trimethylation, but not DNA methylation, is likely to fulfill this role. Intriguingly, although we do detect bivalent domains in pluripotent cells in the early mouse embryo, the epigenetic status of extraembryonic cells does not entirely reflect their in vitro stem cell counterparts. Therefore, differences in epigenetic regulation between lineage progenitors in vivo and in vitro may arise during selection for self-renewal in vitro.

Publication Title

Distinct histone modifications in stem cell lines and tissue lineages from the early mouse embryo.

Sample Metadata Fields

Cell line

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accession-icon SRP069250
OSKM induce extraembryonic endoderm stem (iXEN) cells in parallel to iPS cells
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

While the reprogramming factors OCT4, SOX2, KLF4, and MYC (OSKM) can reactivate the pluripotency network in terminally differentiated cells, they also regulate expression of non-pluripotency genes in other contexts, such as the mouse primitive endoderm. The primitive endoderm is an extraembryonic lineage established alongside the pluripotent epiblast in the blastocyst, and is the progenitor pool for extraembryonic endoderm stem (XEN) cells. Several studies have shown that endodermal genes are upregulated in fibroblasts undergoing reprogramming, although whether endodermal genes promote or inhibit acquisition of pluripotency is unclear. We show that, in fibroblasts undergoing conventional reprogramming, OSKM-induced expression of endodermal genes leads to formation of induced XEN (iXEN) cells, which possess key properties of blastocyst-derived XEN cells, including morphology, transcription profile, self-renewal, and multipotency. Our data show that iXEN cells arise in parallel to iPS cells, indicating that OSKM are sufficient to drive cells to two distinct fates during reprogramming. Overall design: Sequence-based mRNA transcriptional profiling of three different cell lines (MEF, XEN, iXEN) with multiple biological replicates, under two different growth medium conditions (ESC medium, XEN medium) for XEN and iXEN cells.

Publication Title

OSKM Induce Extraembryonic Endoderm Stem Cells in Parallel to Induced Pluripotent Stem Cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE51905
Expression data from differentiated 3T3-L1 pre-adipocytes.
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes.

Publication Title

Inhibition of stearoyl-CoA desaturase-1 in differentiating 3T3-L1 preadipocytes upregulates elongase 6 and downregulates genes affecting triacylglycerol synthesis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE42220
Gene expression data from differentiated 3T3-L1 preadipocytes treated with Palmitic Acid, Stearic Acid, Palmitoleic Acid, or Oleic Acid
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA).

Publication Title

Individual saturated and monounsaturated fatty acids trigger distinct transcriptional networks in differentiated 3T3-L1 preadipocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP073157
RNA Sequencing Data in differentiating mouse embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

ES cell lines were established from mouse embryos, which were homozygous for the Trim33-flox allele and carried the UbcCreERT2 transgene. Cells were cultured without feeder cells in the presence of LIF and 2i. Embryoid bodies (EBs) were generated using the ATCC protocol on low attachment dishes under differentiating conditions. EBs were induced with Tamoxifen at day 4 and harvested at day 7. Overall design: Investigate differentially expressed genes in control and Trim33-deficient embryoid bodies derived from mouse embryonic stem cells

Publication Title

Trim33 is required for appropriate development of pre-cardiogenic mesoderm.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE14640
A condensin-like dosage compensation complex acts at a distance to control expression throughout the genome
  • organism-icon Caenorhabditis elegans
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A condensin-like dosage compensation complex acts at a distance to control expression throughout the genome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14649
DCC binding and function (Expression Analysis)
  • organism-icon Caenorhabditis elegans
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome.

Publication Title

A condensin-like dosage compensation complex acts at a distance to control expression throughout the genome.

Sample Metadata Fields

No sample metadata fields

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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