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accession-icon GSE76968
Myelin-allied gene expression profile of adult neural progenitors shortly after onset of differentiation
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Spontaneous neural repair from endogenous neural stem cells (NSCs) occurs in response to central nervous system (CNS) injuries or diseases to only a limited extent from endogenous NSCs niches. Uncovering the mechanisms that control neural repair and can be further manipulated to promote towards oligodendrocyte progenitors cells (OPCs) and myelinating oligodendrocytes is a major objective.

Publication Title

Prickle1 as positive regulator of oligodendrocyte differentiation.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon GSE3311
Effect of chronic ethanol consumption on rat pancreas
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Male Wistar rats weighing 90-120 g were acclimatized for one week and fed standard laboratory chow, at which time the animals were divided into two groups. Animals were then pair-fed for 8 weeks a regular laboratory chow and water ad libitum or Lieber-DeCarli diet (36% calories from ethanol). Control animals received the iso-caloric amount of dextrose to replace ethanol. After 8 weeks of differential feeding rats were euthanized, the pancreas immediately dissected and stored at -80?C until RNA isolation. RNA expression was analyzed using Affymetrix RAE230A gene chips

Publication Title

Long-term ethanol consumption alters pancreatic gene expression in rats: a possible connection to pancreatic injury.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP186159
Effect of DKK1 on embryo elongation
  • organism-icon Bos taurus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

We report the effect of DKK1 treatment during culture on the length and transcriptome of embryos on day 15 of development, supporting the notion that changes early in development affect later stages of development. Overall design: Bovine embryos were produced in vitro and exposed to either 0 or 100 ng/ml DKK1 from day 5 to 7 of culture. Embryos were transferred on day 7 and recovered on day 15 for evaluation of length and transciptome

Publication Title

Dickkopf-related protein 1 is a progestomedin acting on the bovine embryo during the morula-to-blastocyst transition to program trophoblast elongation.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE21266
Effect of Ursodeoxycholic acid on gene expression in the intestial epithelium
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Background & Aims: Ursodeoxycholic acid (UDCA) attenuates chemical and colitis-induced colon carcinogenesis in animal models. We investigated its mechanism of action on normal intestinal cells, in which carcinogenesis- or inflammation-related alterations do not interfere with the result. Methods: Alterations of gene expression were identified in Affymetrix arrays in isolated colon epithelium of mice fed with a diet containing 0.4% UDCA and were confirmed in the normal rat intestinal cell line IEC-6 by RT-PCR. The effect of the insulin receptor substrate 1 (Irs-1) expression and of ERK phosphorylation on proliferation was investigated in vitro by flow cytometry, western blotting, siRNA-mediated gene suppression or by pharmacological inhibition of the kinase activity. The ERK1-effect on Irs-1 transcription was tested in a reporter system. Results: UDCA-treatment in vivo suppressed potential pro-proliferatory genes including Irs-1 and reduced cell proliferation by more than 30%. In vitro it neutralised the proliferatory signals of IGF-1 and EGF and slowed down the cell cycle. Irs-1 transcription was suppressed due to high ERK1 activation. Both Irs-1 suppression and the persistent high ERK activation inhibited proliferation. Conversely, the decrease of phosphorylation of ERK1 (but not ERK2) or of its expression partially abrogated the inhibitory effects of UDCA. Conclusions: UDCA inhibits proliferation of intestinal epithelial cells by acting upon IGF-1 and EGF pathways and targeting ERK1 and, consequently, Irs-1. The inhibition of these pathways adds a new dimension to the physiological and therapeutic action of UDCA and, since both pathways are activated in inflammation and cancer, suggests new applications of UDCA in chemoprevention and chemotherapy.

Publication Title

UDCA slows down intestinal cell proliferation by inducing high and sustained ERK phosphorylation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE54269
A Molecular Portrait of the Homologous Recombination DNA Repair via Genome-wide Transcriptome Profiling
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE54268
Expression data of ATM, ATR, CHK1, CHK2, and 53BP1 shRNA knockdown and control shRNA in MCF-10A cells
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE54267
Expression data of CHK1 shRNA knockdown and control shRNA in U2OS cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54264
Expression data of Brti1 shRNA knockdown and control shRNA in MCF-10A cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Homologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities Here, we identified an HRD gene signature that robustly predicted HRD status Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information

Publication Title

Genome-wide transcriptome profiling of homologous recombination DNA repair.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP126999
Beta-catenin maintains lung epithelial progenitors after lung specification
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed RNA-seq on human embryonic stem cells raised in an established condition to produce 95% Nkx2.1 cells, with and without withdrawal of Wnt-agonist CHIR99021 or addition of Wnt-inhibitor IWP2 Overall design: Human lung progenitors were derived from RUES2 as described in Huang et al 2014, Huang et al 2015. Wnt agonist withdrawal or addition of Wnt inhibitor was done at day 12, with cell harvest for RNA-seq at day 12 (control) and day 15 (control and treatment)

Publication Title

β-Catenin maintains lung epithelial progenitors after lung specification.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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accession-icon GSE27155
Human thyroid adenomas, carcinomas, and normals
  • organism-icon Homo sapiens
  • sample-icon 99 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Human samples of various thyroid carcinomas, adenomas, and normals, each from a different patient, had mRNA assays performed using Affymetrix HG_U133A arrays, with 22283 probe-sets. The 99 samples consisted of 4 normals, 10 follicular adenomas, 13 follicular carcinomas, 7 oncocytic adenomas, 8 oncocytic carcinomas, 51 papillary carcinomas (each typed as having classical, follicular or tall cell morphology), 4 anaplastic carcinomas, and 2 medullary carcinomas. Interesting additional information on common mutations are provided including RAS mutation, BRAF mutation, RET/PTC rearrangements, and PAX8/PPARG translocations. Details of those assays are provided in our linked publications, as well as additional details on the specific mutations in a few special cases. No survival data is provided. Information for 93 of the 99 samples was previously made available on the web. The anaplastic and medullary carcinoma data were not previously shared. A supplementary Excel spreadsheet holding the same processed data as the series matrix file is provided and is more compact. The raw (.CEL) files are also provided.

Publication Title

Molecular classification of papillary thyroid carcinoma: distinct BRAF, RAS, and RET/PTC mutation-specific gene expression profiles discovered by DNA microarray analysis.

Sample Metadata Fields

Specimen part

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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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