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accession-icon GSE54717
Basonuclin-1 modulates epithelial plasticity and TGF-1-induced loss of epithelial cell integrity
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Basonuclin-1 modulates epithelial plasticity and TGF-β1-induced loss of epithelial cell integrity.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54716
Basonuclin-1 modulates epithelial plasticity and TGF-1-induced loss of epithelial cell integrity [NIAC-NTR]
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

TGF-b1-stimulation induces an epithelial dedifferentiation-process, throughout which epithelial cell sheets disintegrate and gradually switch into fibroblastic-appearing cells (EMT-like transition). The purpose of these profiles was to identify differentially expressed genes that are regulated transcriptionally. Standard microarry-based gene expression profiles measure steady-state RNA but do not provide insight into underlying regulatory principles. NIAC-NTR-based gene expression profiling (Kenzelmann et al., PNAS, 2007) essentially enables the dissection of transcriptionally versus non-transcriptionally regulated genes within respective analysed time-frames. Briefly, NIAC-NTR relies on incorporation of 4sU (thio-uridine) into nascent RNA, which can subsequently be specifically isolated by custom-made columns. Total- and enriched (4sU-labeled) are then further processed for microarray gene expression profiling by standard procedures. This dataset complements previously released data of NIAC-NTR-based gene expression profiling of cells treated with TGF-b1 and 4sU for 2hrs [GSE23833].

Publication Title

Basonuclin-1 modulates epithelial plasticity and TGF-β1-induced loss of epithelial cell integrity.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE54715
Basonuclin-1 modulates epithelial plasticity and TGF-1-induced loss of epithelial cell integrity [BNC1]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

TGF-b1-stimulation induces an epithelial dedifferentiation-process, throughout which epithelial cell sheets disintegrate and gradually switch into fibroblastic-appearing cells (EMT-like transition). Several transcription factors, some of them being TGF-b1-responsive, are functionally involved in such a switch and affect epithelial differentiation and plasticity.

Publication Title

Basonuclin-1 modulates epithelial plasticity and TGF-β1-induced loss of epithelial cell integrity.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE63164
Expression data from Zeb1 knockdown NM18 cells
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Differentiation of epithelial cells is strongly affected by transcription factors related to epithelial to mesenchymal-like progression.

Publication Title

Zeb1 affects epithelial cell adhesion by diverting glycosphingolipid metabolism.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE60127
Perturbation of the Notch pathway in Xenopus laevis embryos
  • organism-icon Xenopus laevis
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

The Notch signaling pathway functions in a number of processes during embryologic development, especially the maintenance or aquisition of cell fate. We purturb the Notch signalling pathway in embryonic Xenopus laevis in order to 1) better characterize the downstream targets of Notch signalling, and 2) determine the extent to which early embryos can recover from transient purturbations to critical signalling pathways, if at all.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062885
Transcriptome seuqnencing of hepatocellular carcinoma(HCC) patients associated with Hepatitis B Virus(HBV)
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Transcriptome seqeunecing on 16 paired HCCs and non-tumorous livers to investigate the effect of HBV integration

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP104418
RNASeq_Fibroblasts_Rapamycin&MethionineRestriction
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

old and young human cardiac fibroblasts plus those treated with rapamycin and methionine restriction or a combination of both

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP070780
RNA-sequencing of metaplastic carcinoma of the breast
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

No description.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon ERP004917
PTEN action in leukemia dictated by the tissue microenvironment
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PTEN encodes a lipid phosphatase that is underexpressed in many cancers owing to deletions, mutations or gene silencing. PTEN dephosphorylates phosphatidylinositol 3,4,5-triphosphate (PIP3), thereby opposing the activity of class I phosphatidylinositol 3-kinases (PI3Ks) that mediate growth and survival factors signaling through PI3K effectors such as AKT and mTOR. To determine whether continued PTEN inactivation is required to maintain malignancy, we generated an RNAi-based transgenic mouse model that allows tetracycline-dependent regulation of PTEN in a time- and tissue-specific manner. Postnatal PTEN knockdown in the hematopoietic compartment produced highly disseminated T-cell leukemia (T-ALL). Surprisingly, reactivation of PTEN mainly reduced T-ALL dissemination but had little effect on tumor load in hematopoietic organs. Lymphoma infiltration into the intestine was dependent on CCR9 G-protein coupled receptor (GPCR) signaling, which was amplified by PTEN loss. Our results suggest that in the absence of PTEN, GPCRs may play an unanticipated role in driving tumor growth and invasion in an unsupportive environment. They further reveal that the role of PTEN loss in tumor maintenance is not invariant and can be influenced by the tissue microenvironment, thereby producing a form of intratumoral heterogeneity that is independent of cancer genotype.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP093363
High-fat diet induced leptin and Wnt expression: RNA-sequencing and pathway analysis of mouse colonic tissue and tumors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Obesity, an immense epidemic affecting approximately half a billion adults, has doubled in prevalence in the last several decades. Epidemiological data support that obesity due to intake of a high-fat, western diet increases the risk of colon cancer; however, the mechanisms underlying this risk remain unclear. Here, utilizing next generation RNA sequencing, we aimed to determine the high-fat diet mediated gene expression profile in mouse colon and the AOM/DSS model of colon cancer.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease, Cell line, Treatment

View Samples
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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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