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accession-icon GSE55490
mTORC1 controls the systemically-induced adaptive regulation of stem cell quiescence into GAlert
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A unique property of many adult stem cells is their ability to exist in a non-cycling, quiescent state. Although quiescence serves an essential role in preserving stem cell function until the stem cell is needed in tissue homeostasis or repair, defects in quiescence can lead to an impairment in tissue function, the extent to which stem cells can regulate quiescence is unknown. Here, we show that the stem cell quiescent state is composed of two distinct functional phases: G0 and an alert phase we term GAlert, and that stem cells actively and reversibly transition between these phases in response to injury-induced, systemic signals. Using genetic models specific to muscle stem cells (or satellite cells (SCs)), we show that mTORC1 activity is necessary and sufficient for the transition of SCs from G0 into GAlert and that signaling through the HGF receptor, cMet is also necessary. We also identify G0-to-GAlert transitions in several populations of quiescent stem cells. Quiescent stem cells that transition into GAlert possess enhanced tissue regenerative function. We propose that the transition of quiescent stem cells into GAlert functions as an 'alerting' mechanism, a novel adaptive response that positions stem cells to respond rapidly under conditions of injury and stress without requiring cell cycle entry or a cell fate commitment.

Publication Title

mTORC1 controls the adaptive transition of quiescent stem cells from G0 to G(Alert).

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE48611
Gene expression of human isogenic trisomy 21 induced pluripotent stem cells and derived neurons
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability, but the precise molecular mechanisms underlying impaired cognition remain unclear. Elucidation of these mechanisms has been hindered by the lack of a model system that contains full trisomy of chromosome 21 (Ts21) in a human genome that enables normal gene regulation. To overcome this limitation,we created Ts21-induced pluripotent stem cells (iPSCs) from two sets of Ts21 human fibroblasts. One of the fibroblast lines had low level mosaicism for Ts21 and yielded Ts21 iPSCs and an isogenic control that is disomic for human chromosome 21 (HSA21). Differentiation of all Ts21 iPSCs yielded similar numbers of neurons expressingmarkers characteristic of dorsal forebrain neurons that were functionally similar to controls. Expression profiling of Ts21 iPSCs and their neuronal derivatives revealed changes in HSA21 genes consistent with the presence of 50% more genetic material as well as changes in non- HSA21 genes that suggested compensatory responses to oxidative stress. Ts21 neurons displayed reduced synaptic activity, affecting excitatory and inhibitory synapses equally. Thus, Ts21 iPSCs and neurons display unique developmental defects that are consistent with cognitive deficits in individuals with Down syndrome and may enable discovery of the underlying causes of and treatments for this disorder.

Publication Title

Deficits in human trisomy 21 iPSCs and neurons.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE17593
Melanoma short-term cultures and cell lines: expression profiling and CNV analyses
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative analysis of the melanoma transcriptome.

Sample Metadata Fields

Disease, Disease stage

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accession-icon SRP000931
Melanoma Cell Transcriptome
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

Paired end sequencing of cDNA isolated from individual melanoma samples via the Illumina sequencing platform to identify genetic aberrations that may play a role in melanoma genesis.

Publication Title

Integrative analysis of the melanoma transcriptome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17349
Expression data for melanoma short-term cultures and cell lines
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

We profiled the gene expression levels from 8 melanoma short-term cultures and 1 melanoma cell line in order to compare to expression level estimates obtained by RNA-seq.

Publication Title

Integrative analysis of the melanoma transcriptome.

Sample Metadata Fields

Disease, Disease stage

View Samples
accession-icon GSE17895
Somatic Mutation Screen of Clear Cell RCC
  • organism-icon Homo sapiens
  • sample-icon 109 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

Systematic sequencing of renal carcinoma reveals inactivation of histone modifying genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE17818
Somatic Mutation Screen of Clear Cell RCC II
  • organism-icon Homo sapiens
  • sample-icon 109 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Systematic somatic mutation screening of 4000 genes in human clear cell renal cell carcinoma. Information on corresponding somatic mutations in each sample can be found at http://www.sanger.ac.uk/genetics/CGP/Studies/.

Publication Title

Systematic sequencing of renal carcinoma reveals inactivation of histone modifying genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE54262
Transcriptome profiling of Bmi1 silenced-K562 CML cell line
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The Bmi1 Polycomb protein is involved in the epigenetic repressive control of self renewal and survival of cancer initiating cells. In Chronic Myeloid Leukemia (CML), bmi1 expression increases gradually as the disease progresses from a chronic latent phase to a deadly blast crisis. We developped an inducible shRNA system to silence Bmi1 in the human K562 chronic myeloid leukemia (CML) cell line in order to identify new Bmi1-target genes.

Publication Title

The BMI1 polycomb protein represses cyclin G2-induced autophagy to support proliferation in chronic myeloid leukemia cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE31760
Transcription profiling wheat responses to adapted and non-adapted isolates of the blast fungus, Magnaporthe
  • organism-icon Triticum aestivum
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

Transcriptional changes were monitored in the wheat cultivar Renan 24 hours post i noculation with adapted and non-adapted Magnaporthe isolates using the Affymetrix wheat genome array GeneChip. Wheat plants cv. Renan were grown in a peat and sand (1:1) mix at 23 C in a Sanyo Fitotron growth cabinet (Sanyo Gallenkamp PLC, Loughborough, U.K.) with a 16/8 h, light/dark cycle. Three Magnaporthe isolates were used in this expt, two wheat-adapted isolates (BR32, BR37) and one wheat non-adapted isolate (BR29). Magnaporthe isolates were grown for eleven days on Complete Media Agar at 25 C under a 16/8h, light/dark cycle. Conidia were harvested by flooding the plates with 5 mL of sterile inoculation solution [0.25% (w/v) gelatine and 0.01% (v/v) Tween 20] and scraping the conidia from the surface using a sterile glass rod. Conidia were filtered through sterile miracloth and the density adjusted to 1 x 10 5 conidia mL-1 with inoculation solution. Fourteen day old wheat seedlings mist inoculated with 4 mL of a Magnaporthe conidia suspension and plants were sealed in plastic propagators to maintain relative humidity c.100% and kept at 25 C in the dark for the first 24 hours post inoculation (hpi). Inoculation solution without Magnaporthe conidia was used as a mock-inoculation control. Leaf samples were collected 24 hpi for transcriptomics analysis from three independent biological experiments. Leaf tissue was ground under liquid nitrogen and total RNA extracted using a QIAquick RNeasy Plant Extraction Kit (Qiagen, Hilden, Germany), followed by TURBO DNaseTM (Ambion, Texas, U.S.A.) treatment. RNeasy Mini Spin column purification (Qiagen) was used to further purify RNA samples for array hybridisation. RNA quality checks, cRNA conversion and Affymetrix genome array hybridisation was carried out by the Nottingham Arabidopsis Stock Centre (NASC) array hybridisation service (http://affymetrix.arabidopsis.info/). ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Graham McGrann. The equivalent experiment is TA24 at PLEXdb.]

Publication Title

Wheat blast: histopathology and transcriptome reprogramming in response to adapted and nonadapted Magnaporthe isolates.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE3653
Inducible Ngn3 Embryonic Stem Cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression of the proendocrine gene neurogenin 3 (Ngn3) is required for the development of pancreatic islets. In order to better characterize the molecular events regulated by Ngn3 during development, we have determined the expression profile of differentiating murine embryonic stem cells (mESCs) uniformly induced to overexpress Ngn3. An ESC line was created that allows for the induction of Ngn3 by adding doxycycline (Dox) to the culture medium. Genome-wide microarray analysis was performed to identify genes regulated by Ngn3 in a variety of both undifferentiated and differentiated conditions. Characterization of pancreatic developmental markers during embryoid body (EB) formation revealed an optimum context for Ngn3 induction. Neuroendocrine genes including neurogenic differentiation 1 (NeuroD1) and single minded 1 (Sim1) were found to be significantly upregulated. Genes regulated by Ngn3 independent of the context were analyzed using systematic gene ontology tools and revealed Notch signaling as the most significantly regulated signaling pathway (p=0.009). This result is consistent with the hypothesis that Ngn3 expression makes the cell competent for Notch signaling to be activated and conversely, more sensitive to Notch signaling inhibition. Indeed, EBs induced to express Ngn3 were significantly more sensitive to gamma-secretase inhibitor-mediated Notch signaling inhibition (p<0.0001). Moreover, we find that Ngn3 induction in differentiating ESCs results in significant increases in insulin, glucagon, and somatostatin transcription.

Publication Title

Differentiation of embryonic stem cells conditionally expressing neurogenin 3.

Sample Metadata Fields

No sample metadata fields

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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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