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accession-icon GSE15680
Laser microdissection of Arabidopsis cells at the powdery mildew infection site
  • organism-icon Arabidopsis thaliana
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

To elucidate host processes and components required for the sustained growth and reproduction of the obligate biotrophic fungus Golovinomyces orontii on Arabidopsis thaliana, laser microdissection was used to isolate cells at the site of infection at 5 days postinfection for downstream global Arabidopsis expression profiling. Site-specific profiling increased sensitivity dramatically, allowing us to identify specific host processes, process components, and their putative regulators hidden in previous whole-leaf global expression analyses. For example, 67 transcription factors exhibited altered expression at the powdery mildew (PM) infection site, with subsets of these playing known or inferred roles in photosynthesis, cold/dehydration responses, defense, auxin signaling, and the cell cycle. Using integrated informatics analyses, we constructed putative regulatory networks for a subset of these processes and provided strong support for host cell cycle modulation at the PM infection site. Further experimentation revealed induced host endoreduplication occurred exclusively at the infection site and led us to identify MYB3R4 as a transcriptional regulator of this process. Induced endoreduplication was abrogated in myb3r4 mutants, and G. orontii growth and reproduction were reduced. This suggests that, by increasing gene copy number, localized endoreduplication serves as a mechanism to meet the enhanced metabolic demands imposed by the fungus, which acquires all its nutrients from the plant host.

Publication Title

Laser microdissection of Arabidopsis cells at the powdery mildew infection site reveals site-specific processes and regulators.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE38822
Gene expression profiling of experimental granulation tissue in Mmp13-/- mice compared to wild type mice
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Proteinases play a pivotal role in wound healing by degrading molecular barriers, regulating cell-matrix interactions and availability of bioactive molecules. Matrix metalloproteinase-13 (MMP-13, collagenase-3) is a wide spectrum proteinase. Its expression and function is linked to the growth and invasion of many epithelial cancers such as squamous cell carcinoma. Moreover, the physiologic expression of MMP-13 is associated e.g. to scarless healing of human fetal skin and adult gingival wounds. While MMP-13 is not found in the normally healing skin wounds in human adults, it is expressed in mouse skin during wound healing. Thus, mouse wound healing models can be utilized for studying the role of MMP-13 in the events of wound healing. As the processes such as the migration and proliferation of keratinocytes, angiogenesis, inflammation and activation of fibroblasts are components of wound repair as well as of cancer, many results received from wound healing studies are also adaptable to cancer research.

Publication Title

MMP-13 regulates growth of wound granulation tissue and modulates gene expression signatures involved in inflammation, proteolysis, and cell viability.

Sample Metadata Fields

Time

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accession-icon GSE108047
Gene expression data from fetal human liver cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Understanding the biological potential of fetal stem/progenitor cells will help define mechanisms in liver development and homeostasis. We isolated epithelial fetal human liver cells and established phenotype-specific changes in gene expression during continuous culture conditions. Fetal human liver epithelial cells displayed stem cell properties with multilineage gene expression, extensive proliferation and generation of mesenchymal lineage cells, although the initial epithelial phenotype was rapidly supplanted by meso-endodermal phenotype in culture. This meso-endodermal phenotype was genetically regulated through cytokine signaling, including transforming growth factor-b, bone morphogenetic protein, fibroblast growth factors, and other signaling pathways. Reactivation of HNF-3a (FOXA1) transcription factor, a driver of hepatic specification in the primitive endoderm, indicated that the meso-endodermal phenotype represented an earlier developmental stage of cells. We found that fetal liver epithelial cells formed mature hepatocytes in vivo, including after genetic manipulation using lentiviral vectors, offering convenient assays for analysis of further cell differentiation and fate. Taken together, these studies demonstrated plasticity in fetal liver epithelial stem/progenitor cells, offered paradigms for defining mechanisms regulating lineage switching in stem/progenitor cells, and provided potential avenues for regulating cell phenotypes for applications of stem/progenitor cells, such as for cell therapy.

Publication Title

Phenotype reversion in fetal human liver epithelial cells identifies the role of an intermediate meso-endodermal stage before hepatic maturation.

Sample Metadata Fields

Specimen part

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accession-icon GSE135000
Expression data from Sprague Dawley rat lenses cultured for 4 days - addition of various inhibitors
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

We created a rat sugar cataract model and examined the effects of various inhibitors on lens clouding. Lenses were removed from 6-week-old SD rats and cultured in M199 medium containing 30 mM galactose.

Publication Title

Histone acetyltransferase and Polo-like kinase 3 inhibitors prevent rat galactose-induced cataract.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP057118
RNA sequencing of heart samples of myotonic dystrophic (DM1) patients
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of alternative splicing in heart (left ventricles) samples of 3 adult DM1 patients versus 3 adult controls Overall design: PolyA RNA from left ventricles (heart) of 3 controls and 3 DM1 patients were analysed by massive parrallel sequencing

Publication Title

Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE67067
Exon array of heart samples of myotonic dystrophic patients
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Analysis of alternative splicing of left ventricles heart samples of 3 DM1 adult versus 3 adult controls

Publication Title

Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP055868
Yap dependent reprogramming of Lgr5+ stem cells drives intestinal regeneration and cancer
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Hippo signalling has been implicated as a key regulator of tissue regeneration. In the intestine, ex vivo organoid cultures model aspects of crypt epithelial regeneration. Therefore in order to uncover the Yap regulated transcriptional programs during crypt regeneration we performed RNA-sequencing of Yap wt and Yap deficient organoids, as well as organoids inducibly expressing Yap. Overall design: Yap loss of function organoids were harvested from Yapfl/fl;VillinCre mice (Yap-/-). In addition, we developed Yap overexpressing organoids by generating a doxycycline-inducible wild-type Yap transgenic line under the control of a Cre driven reverse tetracycline transactivator (rtTA), referred to here as YapTg. Organoids were seeded on day 0 from whole crypts isolated from Yap+/D, YapD/D, YapTg mice and cultured for 24 hours at which time they were harvested for transcriptome analysis by RNAseq.

Publication Title

Yap-dependent reprogramming of Lgr5(+) stem cells drives intestinal regeneration and cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44677
Expression status of mRNA for sex hormone receptors in human dental pulp cells and the response to sex hormones in the cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Objectives: Sex hormone receptors are reported to be present in human dental pulp (HDP) cells. The purpose of this study was to examine the biological significance of estrogen and androgen receptors (ER and AR, respectively) in HDP cells. Design: We isolated HDP cells expressing ER- and AR-mRNAs and investigated the expression status of the receptors and the response to sex hormones in the cells. Results: HDP cells expressing ER- and/or AR-mRNAs had the ability to form alizarin red S-positive nodules in which calcium and phosphorus were deposited in vitro and to differentiate into odontoblasts-like cells and dentin-like tissue in vivo. Individual clones isolated from HDP cells exhibited a different expression pattern of mRNA for ER and AR. Some clones expressed ER- and/or ER-mRNAs and the others coexpressed ER- and AR-mRNAs. Using the Ingenuity software, we found that 17-estradiol (E2) and dihydrotestosterone (DHT) could act directly on HDP cells through ER- or androgen signaling-mediated mechanisms. E2 or DHT stimulated the mRNA expression for genes related to odontogenesis of dentin-containing teeth and odontoblast differentiation, suggesting that ER and AR in HDP cells may be involved in dentinogenesis. Conclusions: Our findings provide new insights into the biological significance of sex hormone receptors in HDP cells.

Publication Title

Expression status of mRNA for sex hormone receptors in human dental pulp cells and the response to sex hormones in the cells.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP015845
Next Generation Sequencing Facilitates Quantitative Analysis of Argonaute 2 (Ago2)-immunoprecipitation (IP) after miR-195 or miR-497 overexpression in HepG2
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

To explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Identification of miR-195 and miR-497 target genes by sequencing Ago2-binding mRNAs and total mRNAs of miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell. Overall design: Deep sequencing of RNAs in Ago2-IP fraction and mRNAs extracted from miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell.

Publication Title

The tumor-suppressive miR-497-195 cluster targets multiple cell-cycle regulators in hepatocellular carcinoma.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

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accession-icon GSE14236
Gene Expression Profiling of the MLL-AF4 and Flt3 tyrosine kinase domain (TKD) genes in 32Dc cell
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The tumorigenesis capacity of MLL-AF4 alone is insufficient for causing leukemia. Based on the finding that an Flt3 gene mutation in the tyrosine kinase domain (TKD) was observed in approximately 15% of MLL leukemia, we investigated synergistic leukemogenesis effects of the two genes in vitro. In a mouse IL3-dependent cell line, 32Dc, the expression of MLL-AF4 and Flt3 TKD was induced using a lentiviral vector. We performed gene expression profiling in the MLL-AF4 and the Flt3 TKD+MLL-AF4 expressing 32Dc cells. The enhancement of Hox genes expression was not identified. However, instead, the expression of S100A6, which was involved in the control of cell proliferation, was synergistically enhanced in the presence of both MLL-AF4 and Flt3 TKD genes.

Publication Title

Multistep pathogenesis of leukemia via the MLL-AF4 chimeric gene/Flt3 gene tyrosine kinase domain (TKD) mutation-related enhancement of S100A6 expression.

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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