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Links from GEO DataSets

Items: 20

1.

Notch signalling mediates secondary senescence

(Submitter supplied) Oncogene induced senescence (OIS) is a tumour suppressive response to oncogene activation that can be transmitted to neighbouring cells through secreted factors of the senescence associated secretory phenotype (SASP). Using single-cell transcriptomics we observed two distinct endpoints, a primary marked by Ras and a secondary by Notch. We find that secondary senescence in vitro and in vivo requires Notch, rather than SASP alone as previously thought. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
4 related Platforms
1163 Samples
Download data: CSV, TXT
Series
Accession:
GSE115301
ID:
200115301
2.

Unbiased identification of CSDE1-regulated targets during oncogene-induced senescence

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL17021
58 Samples
Download data: BED, TXT
Series
Accession:
GSE160002
ID:
200160002
3.

Unbiased identification of CSDE1-regulated targets during oncogene-induced senescence [RNA-Seq-sh]

(Submitter supplied) We show that the RNA-binding protein CSDE1/UNR promotes oncogene-induced senescence (OIS) in primary mouse keratynocytes challenged by over-expression of H-RASv12. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation. Combining individual nucleotide cross-linking and immunoprecipitation (iCLIP), RNA-seq and polysome profiling followed by functional studies, we identify targets regulated by CSDE1 and uncover the downstream molecular mechanisms.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
15 Samples
Download data: TXT
Series
Accession:
GSE160000
ID:
200160000
4.

Unbiased identification of CSDE1-regulated targets during oncogene-induced senescence [RNA-Seq]

(Submitter supplied) We show that the RNA-binding protein CSDE1/UNR promotes oncogene-induced senescence (OIS) in primary mouse keratynocytes challenged by over-expression of H-RASv12. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation. Combining individual nucleotide cross-linking and immunoprecipitation (iCLIP), RNA-seq and polysome profiling followed by functional studies, we identify targets regulated by CSDE1 and uncover the downstream molecular mechanisms.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
9 Samples
Download data: TXT
Series
Accession:
GSE159999
ID:
200159999
5.

Unbiased identification of CSDE1-regulated targets during oncogene-induced senescence [polysome profiling]

(Submitter supplied) We show that the RNA-binding protein CSDE1/UNR promotes oncogene-induced senescence (OIS) in primary mouse keratynocytes challenged by over-expression of H-RASv12. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation. Combining individual nucleotide cross-linking and immunoprecipitation (iCLIP), RNA-seq and polysome profiling followed by functional studies, we identify targets regulated by CSDE1 and uncover the downstream molecular mechanisms.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: TXT
Series
Accession:
GSE159998
ID:
200159998
6.

Unbiased identification of CSDE1-regulated targets during oncogene-induced senescence [i-CLIP]

(Submitter supplied) We show that the RNA-binding protein CSDE1/UNR promotes oncogene-induced senescence (OIS) in primary mouse keratynocytes challenged by over-expression of H-RASv12. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation. Combining individual nucleotide cross-linking and immunoprecipitation (iCLIP), RNA-seq and polysome profiling followed by functional studies, we identify targets regulated by CSDE1 and uncover the downstream molecular mechanisms.
Organism:
Mus musculus
Type:
Other
Platform:
GPL17021
18 Samples
Download data: BED
Series
Accession:
GSE159997
ID:
200159997
7.

Expression data from paracrine senescence

(Submitter supplied) Senescence can be transmitted in a paracrine way from cells undergoing Oncogene Induced Senescence (OIS) to naïve normal cells. We define this phenomenon as “paracrine senescence” We used microarrays to compare the trancriptome of cells undergoing paracrine senescence to the transcriptome of cells suffering OIS to unveil the common signatures defining both events and the similarities between them
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
12 Samples
Download data: CEL
Series
Accession:
GSE41318
ID:
200041318
8.

Oncogene-induced senescence in primary mouse keratinocytes

(Submitter supplied) Analysis of growing or oncogene-induced senescent primary mouse keratinocytes 6 days post infection.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
7 Samples
Download data: TXT
Series
Accession:
GSE93564
ID:
200093564
9.

MLL1 is essential for the senescence-associated secretory phenotype

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below. Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
20 Samples
Download data: BW
Series
Accession:
GSE78142
ID:
200078142
10.

MLL1 is essential for the senescence-associated secretory phenotype [ChIP-Seq]

(Submitter supplied) Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
16 Samples
Download data: BW
Series
Accession:
GSE78141
ID:
200078141
11.

MLL1 is essential for the senescence-associated secretory phenotype [RNA-Seq]

(Submitter supplied) Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: BW
12.

Wnt-signaling potentiates nevogenesis.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL10999 GPL570
18 Samples
Download data: BIGWIG, CEL
Series
Accession:
GSE46818
ID:
200046818
13.

Expression data from 7 Human Melanomas

(Submitter supplied) Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
7 Samples
Download data: BIGWIG
Series
Accession:
GSE46817
ID:
200046817
14.

Expression data from Uninfected and BRAF600V induced melanocytes

(Submitter supplied) Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
2 Samples
Download data: BIGWIG
Series
Accession:
GSE46805
ID:
200046805
15.

Expression data from Control, Uninfected and BRAF infected cells

(Submitter supplied) Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
9 Samples
Download data: CEL
Series
Accession:
GSE46801
ID:
200046801
16.

Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

(Submitter supplied) The aging of pancreatic beta-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging beta-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to beta-cell failure. Herein, we defined the beta-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from human senescent beta-cells. more...
Organism:
Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL28516
27 Samples
Download data: DATA
Series
Accession:
GSE162521
ID:
200162521
17.

SASP signature of beta-cells includes pro-inflammatory and stress response proteins

(Submitter supplied) To define the senescence-associated secretory phenotype (SASP) of beta-cells, we used conditioned media (CM) generated from bleomycin-treated MIN6 cells and from senescent (beta-Gal-positive) primary beta-cells. In order to culture senescent beta-cells, we isolated islet, FACS-sorted them into beta-Gal-positive and negative populations, excluding immune cells through negative selection of CD45-positive and CD11beta-positive cells. more...
Organism:
Homo sapiens; Mus musculus
Type:
Protein profiling by protein array
Platform:
GPL28516
28 Samples
Download data: TXT
Series
Accession:
GSE150285
ID:
200150285
18.

Senescent beta-cells exhibit a unique secretory phenotype that promotes inflammation and remodeling of the extracellular environment

(Submitter supplied) Type 2 Diabetes (T2D) patients have higher proportions of senescent beta-cells than their non-diabetic counterparts (Aguayo-Mazzucato et al., 2019). Senescent beta-cells may propagate dysfunction in neighboring cells through the paracrine effects of the senescence-associated secretory phenotype (SASP). To address the heterogeneity in beta-cell SASP expression and its role in T2D, we measured expression levels of beta-cell SASP signature genes in a mouse model of acute insulin resistance using the insulin receptor antagonist, S961. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
3 Samples
Download data: CSV
Series
Accession:
GSE149984
ID:
200149984
19.

BRD4 connects enhancer remodeling to senescence immune surveillance

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL16791
94 Samples
Download data: BIGWIG
Series
Accession:
GSE74328
ID:
200074328
20.

BRD4 connects enhancer remodeling to senescence immune surveillance (RNA-seq)

(Submitter supplied) 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). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
72 Samples
Download data: TXT
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