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Homo sapiens
8 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes.
Publication Title
The atypical E2F family member E2F7 couples the p53 and RB pathways during cellular senescence.
Sample Metadata Fields
Cell line, Treatment
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Affymetrix Rat Gene 2.0 ST Array (ragene20st)
Description
We identified Ncoa3 as a regulator of neuronal morphology and microRNA activity. In order to uncover target genes of this transcriptional coactivator we performed this microarray analysis.
Publication Title
A large-scale functional screen identifies Nova1 and Ncoa3 as regulators of neuronal miRNA function.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We have examined the effect of suppressing the histone demethylases Jarid1a and Jarid1b on the senescence-associated gene expression signatures.
Publication Title
H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
During development, lineage specification is controlled by several signaling pathways involving various transcription factors (TFs). Here, we studied the RE1-silencing transcription factor (REST) and identified an important role of this TF in cardiac differentiation. Using mouse embryonic stem cells (ESC) to model development, we analyzed the effect of REST knock-out on the ability to these cells to differentiate into the cardiac lineage. Detailed analysis of specific lineage markers expression showed selective down-regulation of endoderm markers in REST-null cells, thus contributing to a loss of cardiogenic signals.
Publication Title
A Role for RE-1-Silencing Transcription Factor in Embryonic Stem Cells Cardiac Lineage Specification.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
Illumina HiSeq 2500
Description
Differential expression patterns of total mRNA in traditionally expanded T cells (vehicle) compared to T cells expanded under drugs (AKT inhibitor and CAL-101) Overall design: Comparison of transcriptional effects of two different drugs
Publication Title
PI3Kδ Inhibition Enhances the Antitumor Fitness of Adoptively Transferred CD8<sup>+</sup> T Cells.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples
GSE43234- Mus musculus
- 11 Downloadable Samples
Illumina mouseRef-8 v1.1 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina mouseRef-8 v1.1 expression beadchip
Description
Analysis of the expression of KH2 embryonic stem cells inducibly expressing V5 tagged Sox17 protein. Results provide information on the endodermal gene expression program activated after Sox17 expression in ES cells.
Publication Title
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 1 Downloadable Sample
- Illumina mouseRef-8 v1.1 expression beadchip
Description
Analysis of the expression of F9 cells after knockdown of Sox7 and Sox17 during their primitive endoderm differnetiation induction with retinoic acid. Results provide information on the endodermal gene expression program regulated by Sox7 and Sox17.
Publication Title
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 72 Downloadable Samples
- IlluminaHiSeq2500
Description
Cellular senescence is a homeostatic program associated with tumor suppression, wound healing, and certain age related pathologies. Senescent cells display a repressive chromatin configuration thought to stably silence proliferation-promoting genes, while at the same time activate an unusual form of immune surveillance involving a secretory program referred to as the senescence-associated secretory phenotype (SASP). Here we demonstrate that senescence also involves a global remodeling of the enhancer landscape with recruitment of the chromatin reader BRD4 to newly activated super-enhancers adjacent to key SASP genes. Transcriptional profiling and functional studies indicate that BRD4 is required for the SASP and downstream paracrine signaling. Consequently, BRD4 inhibition disrupts immune cell-mediated targeting and elimination of premalignant senescent cells in vitro and in vivo. Our results identify a critical role for BRD4-bound super-enhancers in senescence immune surveillance and in the proper execution of a tumor-suppressive program. Overall design: Analysis of RNA isolated from human fibroblasts (IMR90) in proliferating, quiescent or senescent (HrasV12) conditions upon knockdown of Brd4, p65, p53, p53/RB, p16/21 or Vehicle and JQ1 treatment
Publication Title
BRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance.
Sample Metadata Fields
No sample metadata fields
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