Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

ABSTRACT: Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

PROVIDER: PRJNA1009000 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25755121.fastq.gz	Fastqsanger.gz
	SRR25755122.fastq.gz	Fastqsanger.gz
	SRR25755123.fastq.gz	Fastqsanger.gz
	SRR25755124.fastq.gz	Fastqsanger.gz
	SRR25755125.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

Project description:Despite the classical view of senescence as passive growth arrest, it is an active process with profound implications for cellular homeostasis. Indeed, senescent cells remain metabolically active to be able to cope with the energetic demand of the senescence program, although the precise mechanisms underlying this metabolic reprogramming are just beginning to emerge. Here we have identified sin-lncRNA, a previously uncharacterized lncRNA, highly specific of senescent cells, and transcriptionally induced by the master regulator of senescence C/EBPβ. While being strongly activated in senescence, sin-lncRNA knockdown reinforces the senescence program by altering oxidative phosphorylation and impairing mitochondrial function. Sin-lncRNA interacts with the TCA enzyme dihydrolipoamide S-succinyltransferase (DLST) to facilitate its proper function. sin-lncRNA depletion increases DLST nuclear translocation, favoring a metabolic shift from oxidative phosphorylation to a glycolytic phenotype. Moreover, while sin-lncRNA expression remains low in highly proliferative cancer cells, it is strongly induced upon cisplatin-induced senescence. Knockdown of sin-lncRNA in ovarian cancer cells results in deficient oxygen consumption and increased extracellular acidification, sensitizing the cells to cisplatin treatment. Altogether, these results indicate that sin-lncRNA is specifically induced in cellular senescence to maintain metabolic homeostasis. Our findings reveal a new regulatory mechanism in which lncRNA contributes to the adaptive metabolic changes in senescent cells, unveiling the existence of an RNA-dependent metabolic network specific to senescent cells.

2025-04-29 | GSE241620 | GEO

sin-lncRNA interactors in senescent fibroblasts MS

Project description:sin-lncRNA is a noncoding RNA molecule with a role in cellular senescence. In vitro RNA pulldown of biotynilated sin-lncRNA was performed to identify sin-lncRNA specific protein partners

2025-04-29 | PXD044718 | Pride

Expression data from proliferating and senescent IMR90 cells

Project description:Total RNA was isolated from proliferating and senescent IMR90 cells to compare gene-expression to the changes in nucleolus-association in proliferating and senescent IMR90 cells.

2017-06-18 | GSE80447 | GEO

Transcriptomic profiling of irradiated senescent IMR90 cells treated with CDK4/6 or JAK inhibitors

Project description:Human fetal lung fibroblasts (IMR90) were induced to undergo senescence via ionizing radiation (IR). Ten days post-IR, RNA was collected from proliferating, senescent+DMSO, senescent+Palbociclib (2 µM), and senescent+Ruxolitinib (2 µM) conditions. Cells were treated on Days 4, 6, 8 and 10 after IR. This dataset examines how CDK4/6 or JAK inhibition affects gene expression in senescent cells.

2025-08-13 | GSE304272 | GEO

DEG protein in Senescent IMR90

Project description:Differentially regulated protein during IMR90 cell senescence

2024-06-06 | PXD052883 |

Transcription profiling of human IMR90 cells after RNAi suppression of RB, p107 or p130 using in growing, quiescent or ras-induced senescent IMR90 cells

Project description:The action of RB as a tumor suppressor has been difficult to define, in part, due to the redundancy of the related proteins p107 and p130. By coupling advanced RNAi technology to suppress RB, p107 or p130 with a genome wide analysis of gene expression in growing, quiescent or ras-senescent cells, we identified a unique and specific activity of RB in repressing DNA replication as cells exit the cell cycle into senescence, a tumor suppressive program. Experiment Overall Design: Expression profiles of IMR90 cells before and after RNAi-mediated supppression of RB, p107 or p130 in growing, quiescent or ras-induced senescent conditions. RNA was extracted from growing, low serum (0.1% FBS), confluent, or ras-senescent cells.

2010-01-23 | E-GEOD-19864 | biostudies-arrayexpress

Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, with or without TSA treatment.

Project description:Gene expression changes were compared in proliferating and senescent human IMR90 cells, with or without TSA treatment. Method: RNA was extracted, in triplicate, then sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Tophat2 and then analysed with Cufflinks.

2020-06-30 | GSE132370 | GEO

Effect of SMARCA4 knockdown on senescent IMR90 ER:RAS cells

Project description:Effect of SMARCA4 knockdown on senescent IMR90 ER:RAS cells

| PRJNA1047105 | ENA

IMR90 hTERT

Project description:Transcription profiling from young and pre-senescent IMR90 cells, transfected either with hTERT (pBabe-puro-hTERT) or vector control (pBabe-puro). Population doubling values are contained in Characteristics[generation] column.

2014-06-17 | E-MTAB-2087 | biostudies-arrayexpress

Phosphorylation level of SIRT1 in proliferating and senescent IMR90 cells

Project description:Mammalian SIRT1 is a central regulator of metabolism and aging. This project is to analyze global phosphorylation levels of mammalian SIRT1 in proliferating and senescence states using human lung fibroblast IMR90, in order to explore the post-translational regulation of SIRT1 protein upon cellular senescence and its potential roles in the regulatory mechanisms of SIRT1 homeostasis.

2020-09-29 | PXD020081 | Pride

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