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accession-icon GSE24695
Transcription Factor Redundancy Ensures Induction of the Antiviral State
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Transcriptional response to virus infection in mice lacking type I and type III signaling

Publication Title

Transcription factor redundancy ensures induction of the antiviral state.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE51483
Transcriptional Atlas of Cardiogenesis Maps Congenital Heart Disease Interactome
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease.

Publication Title

Transcriptional atlas of cardiogenesis maps congenital heart disease interactome.

Sample Metadata Fields

Age, Specimen part, Cell line

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accession-icon GSE26100
Widespread targeted chromatin remodeling during the initial phase of somatic cell reprogramming
  • organism-icon Mus musculus
  • sample-icon 10 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

Reprogramming factor expression initiates widespread targeted chromatin remodeling.

Sample Metadata Fields

Specimen part

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accession-icon GSE26096
Widespread targeted chromatin remodeling during the initial phase of somatic cell reprogramming [expression]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Despite rapid progress in characterizing transcription factor-driven reprogramming of somatic cells to an induced pluripotent stem (iPS) cell state, many mechanistic questions still remain. To gain insight into the earliest events in the reprogramming process, we systematically analyzed the transcriptional and epigenetic changes that occur during early factor induction after discrete numbers of divisions. We observed rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency or developmentally related gene promoters and enhancers. In contrast, patterns of the repressive H3K27me3 modification remained largely unchanged except for focused depletion specifically at positions where H3K4 methylation is gained. These chromatin regulatory events precede transcriptional changes within the corresponding loci. Our data provide evidence for an early, organized, and population-wide epigenetic response to ectopic reprogramming factors that clarify the temporal order through which somatic identity is reset during reprogramming.

Publication Title

Reprogramming factor expression initiates widespread targeted chromatin remodeling.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP120487
Trnascriptome analysis of HeLa cells infected with rTHOV-wt, -dML, -SW mutant or mock-treated
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of the study was to compare transcriptome changes in HeLa cells after infection with recombinant Thogoto virus (wild-type, ML deletioin mutant or ML SW mutant not able to interact wiith TFIIB. While wild-type virus is able to inhibit inflammatory genes, ML deletion mutant and TFIIB-non-interacting mutant lose this effect on gene transcription. Overall design: Examination of transcriptome changes in HeLa cells under steady state or after THOV infection using Illumina HiSeq.

Publication Title

Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE93940
Intravesical BCG induces CD4+ T Cell Expansion in a Clinically Relevant Immune Competent Model of Bladder Cancer
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

Intravesical BCG Immunotherapy is the standard of care in treating non-muscle invasive bladder cancer, yet its mechanism of action remains elusive. Both innate and adaptive immune responses have been implicated in BCG activity. While prior research has indirectly demonstrated the importance of T cells and shown a rise in CD4+ T cells in bladder tissue after BCG, T cell subpopulations have not been fully characterized. We investigated the relationship between effector and regulatory T cells in an immune competent, clinically relevant rodent model of bladder cancer. Our data demonstrate that cancer progression in the MNU rat model of bladder cancer is characterized by a decline in the CD8/FoxP3 ratio, consistent with decreased adaptive immunity. By contrast, treatment with intravesical BCG leads to a large, transient rise in the CD4+ T cell population in the urothelium, and is both more effective and immunogenic compared to intravesical chemotherapy. Interestingly, whole transcriptome expression profiling of post-treatment intravesical CD4+ and CD8+ T cells revealed minimal differences in gene expression after BCG treatment. Together, our results suggest that while BCG induces T cell recruitment to the bladder, the T cell phenotype does not markedly change, implying that combining T cell activating agents with BCG might improve clinical activity.

Publication Title

Intravesical BCG Induces CD4<sup>+</sup> T-Cell Expansion in an Immune Competent Model of Bladder Cancer.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE14427
Change in expression of genes after retinoic acid treatment of stellate cells
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14426
Change in expression of genes after retinoic acid treatment of stellate cells: time course
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

We evaluated the change in expression of genes after treatment of stellate cells with retinoic acid to understand how the stellate cells can de-differentiate and effect their physiological behaviour in pathological conditions. We then tested the changes in the gene expression in 2D and 3D culture conditions for pancreatic stellate cells and in a pancreatic cancer model.

Publication Title

Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14425
Change in expression of genes after retinoic acid treatment of stellate cells: dose response
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

We evaluated the change in expression of genes after treatment of stellate cells with retinoic acid to understand how the stellate cells can de-differentiate and effect their physiological behaviour in pathological conditions. We then tested the changes in the gene expression in 2D and 3D culture conditions for pancreatic stellate cells and in a pancreatic cancer model.

Publication Title

Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE10300
head and neck squamous cell carcinoma samples
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Patient selection and specimen collection. Thirty-six freshly frozen tumor samples were prospectively collected from patients undergoing surgery or biopsy for HNSCC at the University of North Carolina (UNC) at Chapel Hill (21 patients) and Vanderbilt University (15 patients). All tissues were snap-frozen in liquid nitrogen within 30 minutes of surgical resection or biopsy, and kept at -80oC until further processing. All patients consented to participation in this study under protocols approved by IRB at the two institutions.

Publication Title

A feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle.

Sample Metadata Fields

No sample metadata fields

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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