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accession-icon SRP043192
Escherichia coli strain:DS1 Transcriptome or Gene expression
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Exponentially growing cells and type II persister cells from the DS1-(hipQ)-strain

Publication Title

Novel protocol for persister cells isolation.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon GSE63023
Expression data from heart muscle of cardiac-specific caspase-3 and -7 knockout and wild type newborn and young mice
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Caspases, proteolytic enzymes involved in cell death could play a role independent of cell death in the developing heart

Publication Title

Executioner Caspase-3 and 7 Deficiency Reduces Myocyte Number in the Developing Mouse Heart.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP023469
Global gene expression in the adult Gata6 null mouse pancreas
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We report the global gene expression of mouse pancreatic cells in a pancreas-specific conditional knock-out mouse for Gata6, as compared with age-matched controls. Total RNA was extracted from the pancreas of 6-8 -week old mice of the two genotypes and analyzed. at this age, Gata6P-/- pancreata are histologically normal, but the acinar differentiation programme is already altered. we observe that loss of Gata6 causes the de-repression of ectopic non-pancreatic genes, as well as some genes involved in the mesenchymal programme. Overall design: mRNA extracted from the pancreas of 4 controls and 4 Gata6P-/- mice was sequenced.

Publication Title

The acinar regulator Gata6 suppresses KrasG12V-driven pancreatic tumorigenesis in mice.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE56615
Expression data from human breast cancer cells MDA-MB-231-Luc knockdown for RRAS2 expression.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We used microarrays to investigate gene expression changes induced by the inhibition of RRAS2 expression using shRNA techniques to stably knockdown the endogenous transcripts of this GTPase in human MDA-MB-231-Luc cells.

Publication Title

Contribution of the R-Ras2 GTP-binding protein to primary breast tumorigenesis and late-stage metastatic disease.

Sample Metadata Fields

Cell line

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accession-icon SRP041005
Transcriptional profiles by deep sequencing (RNA-seq) of papillomas generated using the DMBA/TPA protocol from control and transgenic Nanog overexpressing mice
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

NANOG is a key pluripotency factor in embryonic stem cells that is frequently expressed in squamous cell carcinomas (SCCs). However, a direct link between NANOG and SCCs remains to be established. Here, we show that inducible overexpression of NANOG in mouse skin epithelia dramatically promotes the formation of carcinomas upon chemical carcinogenesis. Gene expression analyses in pre-malignant skin indicate that NANOG induces a large set of genes associated to stemness and to epithelial-mesenchymal transition (EMT). Overall design: 4 papillomas from different control mice (CTR), and 3 papillomas from different transgenic Nanog overexpressing mice (TG)

Publication Title

The pluripotency factor NANOG promotes the formation of squamous cell carcinomas.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP025986
Transcriptome analysis of Germinal Center and naïve B cells from miR-217TG and control mice by RNAseq
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

microRNAs (miRNAs) regulate virtually all biological processes, but little is known of their role in germinal center (GC) B cells. While the GC reaction is crucial to ensure a competent immune response, GC B cells are also the origin of most human lymphomas. Here we report that miR-217 is specifically upregulated in GC B cells. Gain- and loss-of-function mouse models reveal that miR-217 functions as a positive modulator of the GC response through the regulation of a DNA repair gene network. Moreover, we show that miR-217 overexpression promotes mature B cell lymphomagenesis. Therefore miR-217 provides a novel molecular link between the normal GC response and B cell transformation Overall design: 4 samples were analyzed by RNAseq: 1) naïve (CD19+Fas-GL7-) B cells from miR-217TG, 2) GC (CD19+Fas+GL7+) B cells from miR-217TG, 3) naïve (CD19+Fas-GL7-) B cells from littermate controls and 4) GC (CD19+Fas+GL7+) B cells from littermate controls. Samples were isolated by cell sorting from pooled Peyer’s patches (4-6 animals per genotype). Two independent experiments were performed.

Publication Title

miR-217 is an oncogene that enhances the germinal center reaction.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP026364
Transcriptional profiles by deep sequencing (RNA-seq) of in vivo-generated mouse iPSCs, in vitro-generated mouse iPSCs, and mouse ESCs
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We have generated “reprogrammable” transgenic mice that ubiquitously express the four Yamanaka factors in an inducible manner. Transitory induction of the transgene results in multiple teratomas emerging from a variety of organs, thus indicating that full reprogramming into iPSCs can occur in vivo. By performing bone marrow transplant experiments, we demonstrate that both hematopoietic cells, as well as non-hematopoietic cells can be reprogrammed in vivo. Remarkably, reprogrammable mice also present circulating iPSCs in the bloodstream (in vivo-iPSCs) with all the expected properties of bona fide iPSCs. Moreover, in contrast to in vitro-iPSCs or embryonic stem cells (ESCs), in vivo-iPSCs have an increased capacity to undergo trophectoderm lineage differentiation, which suggests that in vivo-iPSCs are more plastic or primitive than in vitro-generated iPSCs or ESCs. Overall design: 6 clones of in vivo-generated iPSCs, 5 indendent clones of in vitro-generated iPSCs, and 3 clones of established ESCs

Publication Title

Reprogramming in vivo produces teratomas and iPS cells with totipotency features.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP149483
RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the reporter gene LacZ (located next to the oncogene in the same polycistronic mRNA), by loading CD31-/CD45- pneumocytes with the LacZ-activated fuorogenic molecule FDG prior to FACS sorting. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.

Publication Title

Sirt1 protects from K-Ras-driven lung carcinogenesis.

Sample Metadata Fields

Subject

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accession-icon SRP149487
RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen and 2 weeks of chase
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment plus 2 weeks without tamoxifen. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the fluorescent reporter gene Katushka (located at an independent locus), by detecting Katushka fluorescence. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.

Publication Title

Sirt1 protects from K-Ras-driven lung carcinogenesis.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE45120
Gene expression from H69M versus H69 SCLC cell lines
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

H69M cells derive from H69 small cell lung cancer cells subjected to prolonged treatment with HGF. Among the whole population of cells, a subset of more fibroblastic cells was isolated (H69M-mesenchymal). In this experiment we compared expression profiles of both cell lines

Publication Title

Targeting epithelial-to-mesenchymal transition with Met inhibitors reverts chemoresistance in small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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