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accession-icon GSE37396
The histone methyltransferase MLL3 regulates genome-scale circadian transcription
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone methyltransferase MLL3 contributes to genome-scale circadian transcription.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE107458
Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE107446
Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes [expression]
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Primary cell cultures were isolated from KrasG12D-driven, PiggyBac transposon-transposase pancreatic cancer cell cultures and subjected to microarray-based expression profiling for the investigation of expression profiles.

Publication Title

Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP121007
Oncogenic Role of THOR, a Conserved Cancer/Testis Long Noncoding RNA
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Large scale transcriptome sequencing efforts have vastly expanded the catalog of long non-coding RNAs (lncRNAs) with varying evolutionary conservation, lineage expression, and cancer specificity. Here we functionally characterize a novel ultraconserved lncRNA, THOR (ENSG00000226856), which exhibits expression exclusively in testis and a broad range of human cancers. THOR knockdown and overexpression in multiple cell lines and animal models alters cell or tumor growth supporting an oncogenic role. We discovered a conserved interaction of THOR with IGF2BP1 and show that THOR contributes to the mRNA stabilization activities of IGF2BP1. Notably, transgenic THOR knockout produced fertilization defects in zebrafish and also conferred a resistance to melanoma onset. Likewise, ectopic expression of human THOR in zebrafish accelerated the onset of melanoma. THOR represents a novel class of functionally important cancer/testis lncRNAs whose structure and function have undergone positive evolutionary selection.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP135850
Transcriptomic characterization of FTD-resistant colorectal cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Examination of mRNA expression levels of parental cell line and FTD resistant cell line.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE21723
Expression profiling of vascular endothelial cells using minimal input material
  • organism-icon Homo sapiens
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Expression profiling using minimal endothelial cell numbers isolated from 2 phenotypic groups (condition A and B). In total 64 GeneChips were processed, 12 Genechips for condition A and 52 GeneChips for condition B.

Publication Title

No associated publication

Sample Metadata Fields

Age

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accession-icon GSE57008
Transcriptomics of murine ex vivo isolated alveolar type 2 epithelial cells from Influenza A respiratory infection
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Influenza A virus (IAV) infections periodically cause substantial morbidity and mortality in the human population. In the lung, the primary targets for IAV replication are type II alveolar epithelial cells (AECII), which are increasingly recognized for their immunological potential. However, our knowledge of the role of AECII in anti-IAV immunity is incomplete and their in vivo response to infection has not been evaluated. To increase our understanding of their role in host-response to IAV-infection, we analyzed transcriptional regulation in primary AECII isolated from infected mice. Results: Microarray analyses of AECII isolated on the first three days following IAV-infection revealed extensive transcriptional regulation. A multitude of differentially expressed transcripts was identified and in comparison to whole-lung tissue revealed a strong contribution of AECII to respiratory anti-IAV responses. Type I interferon played a major role in the detected gene expression profile and functional pathway analyses showed AECII to be highly active in pathogen recognition, cell recruitment and antigen-presentation. Analysis of Toll-like receptor 7 (TLR7) deficient mice indicated AECII to rely on the hosts expression of this innate IAV-sensor to elicit their full response. Importantly, the AECII transcriptional profiles correlated to cell recruitment and type I interferon levels detected in the lungs of infected animals. Conclusions: Ex vivo analysis of primary murine AECII proved as a powerful tool to increase our understanding of AECII biology in infection. Our analysis revealed an exceptionally strong contribution of AECII to local host defenses by integrating signals provided by surrounding cells and direct pathogen recognition.

Publication Title

Alveolar Type II Epithelial Cells Contribute to the Anti-Influenza A Virus Response in the Lung by Integrating Pathogen- and Microenvironment-Derived Signals.

Sample Metadata Fields

Treatment

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accession-icon GSE35959
Effects of aging, primary osteoporosis, and cellular senescence on Human Mesenchymal Stem Cells
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The transcriptional profile of mesenchymal stem cell populations in primary osteoporosis is distinct and shows overexpression of osteogenic inhibitors.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE17302
IFN-mediated gene expression patterns
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE197751
Cigarette smoke extract disturbs mitochondria-regulated airway epithelial cell responses to pneumococci
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.

Publication Title

Cigarette Smoke Extract Disturbs Mitochondria-Regulated Airway Epithelial Cell Responses to Pneumococci.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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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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