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accession-icon GSE144397
AP-1 imprints a reversible transcriptional programme of senescent cells
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Senescent cells affect many physiological and pathophysiological processes. While select genetic and epigenetic elements for senescence induction have been identified, the dynamics, epigenetic mechanisms and regulatory networks defining senescence competence, induction and maintenance remain poorly understood, precluding the deliberate therapeutic targeting of senescence for health benefits. Here, we examined the possibility that the epigenetic state of enhancers determines senescent cell fate. We explored this by generating time-resolved transcriptomes and epigenome profiles during oncogenic RAS-induced senescence and validating central findings in different cell biology and disease models of senescence. Through integrative analysis and functional validation, we reveal links between enhancer chromatin, transcription factor recruitment and senescence competence. We demonstrate that activator protein 1 (AP-1) ‘pioneers’ the senescence enhancer landscape and defines the organizational principles of the transcription factor network that drives the transcriptional programme of senescent cells. Together, our findings enabled us to manipulate the senescence phenotype with potential therapeutic implications.

Publication Title

AP-1 imprints a reversible transcriptional programme of senescent cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

View Samples
accession-icon GSE134753
Expression data from treatment-induced senescence in mouse Emu-myc B-cell lymphoma model.
  • organism-icon Mus musculus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment.

Publication Title

AP-1 imprints a reversible transcriptional programme of senescent cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE143248
AP-1 Imprints a Reversible Transcriptional Programme of Senescent Cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Senescent cells affect many physiological and pathophysiological processes. While select genetic and epigenetic elements for senescence induction have been identified, the dynamics, epigenetic mechanisms and regulatory networks defining senescence competence, induction and maintenance remain poorly understood, precluding the deliberate therapeutic targeting of senescence for health benefits. Here, we examined the possibility that the epigenetic state of enhancers determines senescent cell fate. We explored this by generating time-resolved transcriptomes and epigenome profiles during oncogenic RAS-induced senescence and validating central findings in different cell biology and disease models of senescence. Through integrative analysis and functional validation, we reveal links between enhancer chromatin, transcription factor recruitment and senescence competence. We demonstrate that activator protein 1 (AP-1) 'pioneers' the senescence enhancer landscape and defines the organizational principles of the transcription factor network that drives the transcriptional programme of senescent cells. Together, our findings enabled us to manipulate the senescence phenotype with potential therapeutic implications.

Publication Title

AP-1 imprints a reversible transcriptional programme of senescent cells.

Sample Metadata Fields

Cell line, Treatment, Time

View Samples
accession-icon SRP201482
RNA sequencing comparing normal and premalignant EuMyc B220+ cells in Max WT and conditional Max KO mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study was to compare expression profiles of B cells in the presence and absence of transcription factor MAX under normal and premalignant settings Overall design: Each genotype is represented in triplicate (cells isolated from 3 individual mice for each)

Publication Title

<i>Max</i> deletion destabilizes MYC protein and abrogates Eµ-<i>Myc</i> lymphomagenesis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE95286
Expression data of undifferentiated cells and xenografts of human pluripotent stem cells and embryonal carcinoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 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

Differentiation-Defective Human Induced Pluripotent Stem Cells Reveal Strengths and Limitations of the Teratoma Assay and In Vitro Pluripotency Assays.

Sample Metadata Fields

Specimen part

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accession-icon GSE95285
Xenografts of human pluripotent stem cells and embryonal carcinoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Here we perfomed the Teratoma assay for a normal human embryonic stem cell line (H9(+Dox)), a human embryonic stem cell line with a mesendodermal differentiation bias (H9Hyb), a normal human induced pluripotent stem cell line (LU07), a human induced pluripotent stem cell line with reactivated transgenes (LU07+Dox) and a human embryonal carcinoma cell line (EC) and anayzed their gene expression.

Publication Title

Differentiation-Defective Human Induced Pluripotent Stem Cells Reveal Strengths and Limitations of the Teratoma Assay and In Vitro Pluripotency Assays.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE65997
The Nicotinic alpha6 Subunit Gene Determines Variability in Chronic Pain Sensitivity and Nicotine Anti- allodynia via Cross-inhibition of P2X2/3 Receptors.
  • organism-icon Mus musculus
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarray-based expression genomics in 25 inbred mouse strains to identify dorsal root ganglion (DRG)-expressed genetic contributors to mechanical allodynia a prominent symptom of chronic pain.

Publication Title

The nicotinic α6 subunit gene determines variability in chronic pain sensitivity via cross-inhibition of P2X2/3 receptors.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE20674
Nascent mRNA profiling of LPS-stimulated mouse macrophages
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To identify transcriptionally regulated genes in primary mouse macrophages stimulated with LPS with high sensitivity, we isolated nascent RNA following metabolic labelling with 4-thiouridine during the last 35 min before cell harvest, as recently described (Dolken et al. 2008 RNA 14:1959-72). Microarray analyses of nascent RNA identified substantially more probe sets as up-regulated after 45 min of LPS stimulation than parallel analyses of total cellular RNA. In contrast, 4.5 h after stimulation, up-regulated genes in total and nascent RNA largely overlapped. This approach therefore allowed a much more sensitive detection of early changes in transcription, and the respective genes are likely to be direct targets of LPS-regulated transcription factors.

Publication Title

The phosphoproteome of toll-like receptor-activated macrophages.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE69886
Expression data from control, aged and activated neutrophils in mouse blood
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neutrophils provide immune protection against pathogens but also may promote tissue injury in inflammatory diseases. Although neutrophils are generally considered as a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and the replenishment by newly released neutrophils from the bone marrow.

Publication Title

Neutrophil ageing is regulated by the microbiome.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE92698
Precipitation of mRNAs by Ago2 and phosphorylation mutants
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Argonaute (Ago) proteins associate with microRNAs (miRNAs), which guide them to complementary target mRNAs resulting in gene silencing.

Publication Title

Phosphorylation of Argonaute proteins affects mRNA binding and is essential for microRNA-guided gene silencing &lt;i&gt;in vivo&lt;/i&gt;.

Sample Metadata Fields

Cell line

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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