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accession-icon GSE68133
Prox1 downregulation is a prerequisite for the maturation and expansion of postnatal murine beta cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Alterations in the expression of key transcription factors can be harmful for pancreatic beta cell homeostasis and could lead to diabetes. This study uncovered that Prox1 overexpression obstructs beta cell maturation and results in severe hyperglycemia.

Publication Title

Lack of Prox1 Downregulation Disrupts the Expansion and Maturation of Postnatal Murine β-Cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE45222
Reversible mRNA and miRNA expression patterns in the transcriptome of Rasless fibroblasts
  • organism-icon Mus musculus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of the transcriptional profiles of mRNA and microRNA in Rasless fibroblasts. 4-Hydroxy-tamoxifen (4-OHT) treatment triggers removal of K-Ras expression in [H-Ras-/-;N-Ras-/-;K-Raslox/lox;RERTert/ert ] mouse fibroblasts (named K-Raslox) generating Rasless MEFs which are unable to proliferate, but recover proliferative ability after ectopic expression of constitutively active downstream kinases such as BRAF and MEK1.

Publication Title

Reversible, interrelated mRNA and miRNA expression patterns in the transcriptome of Rasless fibroblasts: functional and mechanistic implications.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE6850
A dominant negative form of cJun affects genes that have opposing effects on lipid homeostasis in mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

cJun is a transcription factor activated by phosphorylation by SAPK/JNK MAP kinase pathway that has been linked to atherosclerosis. Adenovirus mediated gene transfer of a dominant negative form of cJun in C57BL/6 mice increased greatly the apolipoprotein E (ApoE) mRNA and plasma apoE levels and induced dyslipidmia, characterized by increased plasma cholesterol, triglyceride and VLDL levels and accumulation of discoidal HDL particles. Unexpectedly, infection of ApoE-/- mice with adenovirus expressing dn-cJun reduced by 50% plasma cholesterol, suggesting that the dn-cJun affected other genes that control plamsa cholesterol. To determine the molecular pathways implicated in this process we performed whole genome expression profiling using total RNA from the liver of infected ApoE-/- mice.

Publication Title

A dominant negative form of the transcription factor c-Jun affects genes that have opposing effects on lipid homeostasis in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP017378
Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) in proliferation, quiescence, senescence and transformed states.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells under the following conditions: normal proliferation, quiescence (induced by serum depletion), senescence (induced by activation of the oncogenic RASG12V gene, and examined at early (5 days; pre-senescent state) and late (14 days; fully senescent state) time points), and neoplastic transformation (induced by RASG12V in the background of stable p53 and p16INK4A knockdowns and SV40 small-T expression. Overall design: RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed. Ribosome profiling, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed.

Publication Title

p53 induces transcriptional and translational programs to suppress cell proliferation and growth.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP020544
Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) of BJ cells treated with Nutlin-3a, an MDM2 inhibitor, which induces p53.
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells in which p53 was induced by Nutlin-3a Overall design: RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs Ribosome profiling was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs

Publication Title

p53 induces transcriptional and translational programs to suppress cell proliferation and growth.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP093668
Transcriptome analysis of murine T-cell lymphoblastic lymphomas induced by HrasG12V, p53 KO and CIC loss-of-function
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA sequencing of T-ALL tumors derived from genetically modified mouse models: CIC loss-of-function, HRASG12V driven from the Kras promoter and Trp53 KO. Results provide insight into the role of the RAS/CIC axis in T-ALL development. Overall design: RNA-Sequencing of 5 CIC LOF, 3 K:HrasG12V and 4 Trp53 KO T-ALL murine tumor samples.

Publication Title

Inactivation of Capicua in adult mice causes T-cell lymphoblastic lymphoma.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE20076
BRD7 is a candidate tumour suppressor gene required for p53 function
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS.

Publication Title

BRD7 is a candidate tumour suppressor gene required for p53 function.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon SRP078433
Transcriptome Profile of Lung Dendritic Cells after In Vitro Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Infection
  • organism-icon Sus scrofa
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Investigation of the transcriptome profile of lung dendritic cells (DCs) of two genetically different pig breeds (Pietrain and Duroc) after PRRSV infection in vitro and determination of the temporal changes in transcriptional profiles. Overall design: Pietrain and Duroc lung DCs were isolated and infected in vitro with PRRSV. Total cellular mRNA from non-infected (0 hours) and infected (3, 6, 9, 12 and 24 hours post infection) lung DCs was extracted and 12 lung DCs samples were used for the global transcriptome profile analysis (RNA-Seq).

Publication Title

Transcriptome profile of lung dendritic cells after in vitro porcine reproductive and respiratory syndrome virus (PRRSV) infection.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon SRP007596
Genome-wide maps of polyadenylation sites in control and PABPN1kd cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII, IlluminaHiSeq2000

Description

We applied deep-sequencing based technique, 3''-Seq, to obtain comprehansive maps of poly-A sites in human cells. 3''-Seq was applied to two cell lines (U2OS and RPE-1), in control and PABPN1 knockdown cells Overall design: Examination of poly-A sites in control and PABPN1kd cells (in two different cell lines)

Publication Title

The poly(A)-binding protein nuclear 1 suppresses alternative cleavage and polyadenylation sites.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41212
Arabidopsis thaliana seed germination timecourse
  • organism-icon Arabidopsis thaliana
  • sample-icon 116 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

This series analyses germinating Arabidopsis seeds with both temporal and spatial detail, revealing two transcriptional phases that are separated with respect to testa rupture. Performed as part of the ERA-NET Plant Genomics grant vSEED.

Publication Title

Transcriptional dynamics of two seed compartments with opposing roles in Arabidopsis seed germination.

Sample Metadata Fields

Specimen part, Time

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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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