Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-61130

ABSTRACT: Analysis of the senescent transcriptome upon expression of a ZFP36L1 phosphomutant

OTHER RELATED OMICS DATASETS IN: PRJNA260300

PROVIDER: E-GEOD-61130 | ExpressionAtlas | 2019-05-14

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-61130-analysis-methods.tsv	Tabular
	E-GEOD-61130-analytics.tsv	Tabular
	E-GEOD-61130-analytics.tsv.undecorated	Tabular
	E-GEOD-61130-analytics.tsv.undecorated.unrounded	Tabular
	E-GEOD-61130-analytics.tsv.unrounded	Tabular

Items per page:

1 - 5 of 105

Similar Datasets

Homo sapiens

Project description:Analysis of the senescent transcriptome upon expression of a ZFP36L1 phosphomutant

| PRJNA260300 | ENA

Homo sapiens

Project description:Transcriptomic analysis of senescent cells upon EXOC7 knockdown.

| PRJNA395378 | ENA

Homo sapiens

Project description:Transcriptomic analysis of senescent cells upon PTBP1 knockdown.

| PRJNA395363 | ENA

Analysis of the senescent transcriptome upon expression of a ZFP36L1 phosphomutant

Project description:We expressed either a wt or a phosphomutant version of ZFP36L1 in IMR90 ER:RAS cells. 7 days upon RAS induction (when the cells reach a fully senescent phenotype) we collected the RNA. ZFP36L1 is a RNA binding protein that binds to AU-rich elements in the 3âUTR of mRNAs and triggers their degradation. Our previous experiments showed that the activity of ZFP36L1 was key in the regulation of the senescent phenotype.By performing RNAseq we have uncovered the effect of expressing a constitutively active mutant of ZFP36L1 within the senescent transcriptome. 4 samples examined: Non-senescent cells (EV - 4OHT), Senescent cells (EV + 4OHT), Senescent cells expressing ZFP36L1wt and Senescent cells expressing ZFP36L1mut

2015-07-07 | E-GEOD-61130 | biostudies-arrayexpress

Senescent Characteristics of Human Corneal Endothelial Cells upon Ultraviolet-A Exposure

Project description:Purpose: The objective of this study was to investigate the senescent phenotypes of human corneal endothelial cells (hCEnCs) upon treatment with ultraviolet (UV)-A. Methods: We assessed cell morphology, senescence-associated β-galactosidase (SA-β-gal) activity, cell proliferation and expression of senescence markers (p16 and p21) in hCEnCs exposed to UV-A radiation, and senescent hCEnCs induced by ionizing radiation (IR) were used as positive controls. We performed RNA sequencing and proteomics analysis to compare gene and protein expression profiles between UV-A- and IR-induced senescent hCEnCs, and we also compared the results to non-senescent hCEnCs. Results: Cells exposed to 5 J/cm2 of UV-A or to IR exhibited typical senescent phenotypes, including enlargement, increased SA-β-gal activity, decreased cell proliferation and elevated expression of p16 and p21. RNA-Seq analysis revealed that 83.9% of the genes significantly upregulated and 82.6% of the genes significantly downregulated in UV-A-induced senescent hCEnCs overlapped with the genes regulated in IR-induced senescent hCEnCs. Proteomics also revealed that 93.8% of the proteins significantly upregulated in UV-A-induced senescent hCEnCs overlapped with those induced by IR. In proteomics analyses, senescent hCEnCs induced by UV-A exhibited elevated expression levels of several factors part of the senescence-associated secretory phenotype. Conclusion: In this study, where senescence was induced by UV-A, a more physiological stress for hCEnCs compared to IR, we determined that UV-A modulated the expression of many genes and proteins typically altered upon IR treatment, a more conventional method of senescence induction, even though UV-A also modulated specific pathways unrelated to IR.

2024-05-17 | GSE250224 | GEO

Transcriptomic analysis of senescent cells upon PTBP1 knockdown and EXOC7 knockdown

Project description:Transcriptomic analysis of senescent cells upon PTBP1 knockdown and EXOC7 knockdown

| PRJNA395374 | ENA

Analysis of the senescent transcriptome upon expression of a ZFP36L1 phosphomutant

Project description:We expressed either a wt or a phosphomutant version of ZFP36L1 in IMR90 ER:RAS cells. 7 days upon RAS induction (when the cells reach a fully senescent phenotype) we collected the RNA. ZFP36L1 is a RNA binding protein that binds to AU-rich elements in the 3’UTR of mRNAs and triggers their degradation. Our previous experiments showed that the activity of ZFP36L1 was key in the regulation of the senescent phenotype.By performing RNAseq we have uncovered the effect of expressing a constitutively active mutant of ZFP36L1 within the senescent transcriptome.

2015-07-07 | GSE61130 | GEO

Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts [miRNA]

Project description:To study and correlate modulations of miRNome with modifications of transcriptome in human stress-induced senescent fibroblasts, Agilent microarrays data were compared by bioinformatics analysis with a focus on ECM components. We identified two unreported direct interactions since we highlighted a reduction in the expression of both miR-22-5p and -199a-5p in senescent fibroblasts, correlated to an increase of MMP1 expression.

2022-01-09 | GSE77406 | GEO

Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts [mRNA]

2022-01-09 | GSE77074 | GEO

Cellular proteostasis collapse in mammalian senescence

Project description:Proteostasis collapse, the diminished ability to maintain protein homeostasis, has been established as a hallmark of nematode aging. However, whether proteostasis collapse occurs in humans has remained unclear. Here, we demonstrate that proteostasis decline is intrinsic to human senescence. Using transcriptome-wide characterization of gene expression, splicing, and translation, we found a significant deterioration in the transcriptional activation of the heat shock response in stressed senescent cells. Furthermore, phosphorylated HSF1 nuclear localization and distribution were impaired in senescence. Interestingly, alternative splicing regulation was also dampened. Surprisingly, we found a decoupling between different unfolded protein response (UPR) branches in stressed senescent cells. While young cells initiated UPR-related translational and transcriptional regulatory responses, senescent cells showed enhanced translational regulation and endoplasmic reticulum (ER) stress sensing; however, they were unable to trigger UPR-related transcriptional responses. This was accompanied by diminished ATF6 nuclear localization in stressed senescent cells. Finally, we found that proteasome function was impaired following heat stress in senescent cells, and did not recover upon return to normal temperature. Together, our data unraveled a deterioration in the ability to mount dynamic stress transcriptional programs upon human senescence with broad implications on proteostasis control and connected proteostasis decline to human aging.

2020-12-09 | GSE124609 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data