Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mutual regulation between GDF11 and TET2 prevents senescence in adipose tissue-derived mesenchymal stem cells

ABSTRACT: Mutual regulation between GDF11 and TET2 prevents senescence in adipose tissue-derived mesenchymal stem cells

PROVIDER: PRJNA598214 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10806365.fastq.gz	Fastqsanger.gz
	SRR10806366.fastq.gz	Fastqsanger.gz
	SRR10806367.fastq.gz	Fastqsanger.gz
	SRR10806368.fastq.gz	Fastqsanger.gz
	SRR10806369.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Mutual regulation between GDF11 and TET2 prevents senescence in adipose tissue-derived mesenchymal stem cells

Project description:We implemented transcriptomic analyses of hADSCs treated with rGDF11 1, 2 and 6 days

2022-12-31 | GSE142761 | GEO

Effect of GDF11 on RANKL-induced osteoclastogenesis

Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow-derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment. Mouse BMMs were treated with or without GDF11 for RNA extraction and and hybridization on Affymetrix microarrays

2016-07-21 | E-GEOD-84609 | biostudies-arrayexpress

Inhibiting or depleting AHCY prevents senescence induction

Project description:Inhibiting or depleting AHCY prevents senescence induction

| PRJNA656198 | ENA

RNAseq of wild type and GDF11-/- Neuro-2a cells

Project description:Growth differentiation factor 11 (GDF11), is one of the members of transforming growth factor β (TGFβ) superfamily. We set out to unequivocally reveal the effect of endogenous GDF11 on biological process by adopting CRISPR/Cas9 gene knockout strategy to specifically delete GDF11 gene in Neuro-2a cells. We analyze mRNA profiles of differentially genes in wild type (WT) and GDF11 knockout (GDF11-/-) Neuro-2a cells by using RNA-seq technology. The RNA-seq data reported here provide a fundamental materials and evidence for investigations of biological function of GDF11.

2021-10-06 | GSE167538 | GEO

Effect of GDF11 on RANKL-induced osteoclastogenesis

Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow–derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment.

2016-07-21 | GSE84609 | GEO

Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle

Project description:In this study, we investigated signaling pathways in Skeletal muscle precursors that are altered with aging and age-related deficits in muscle regenerative potential. We performed fluorescence activated cell sorting (FACS) to obtain highly purified skeletal muscle satellite cells from young, middle-aged and old mice. Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction. We used Affymetrix Mouse Genome array to identify global transcriptional changes associated with age in skeletal muscle precursors.

2014-05-08 | E-GEOD-50821 | biostudies-arrayexpress

GDF11 is a myokine that inhibits muscle differentiation and induces atrophy during regeneration

Project description:Age-related frailty may in part be due to a decreased competency in skeletal muscle regeneration. The role of the closely related TGFbeta amily molecules myostatin and GDF11 in regeneration is unclear. The commercially available antibody which in a prior report was used to demonstrate an age-related decrease in GDF11 was found to detect both GDF11 and myostatin, and with this reagent it appears that the combination of GDF11 and myostatin increases with age in serum. Mechanistically, GDF11 and myostatin induce SMAD2/3 phosphorylation, and both inhibit myoblast differentiation and regulate identical downstream signaling. GDF11 injected into adult mice in a model of regeneration induces an increase in smaller fibers and a decrease in satellite cell expansion. There are no signs of benefit from GDF11 to regeneration. Thus, GDF11 appears to be an age-associated myokine that inhibits muscle differentiation, and is thus a target for blockade to treat frailty

2015-05-20 | GSE67326 | GEO

Deficiency of GDF11 Accelerates TAC-Induced Heart Failure by impairing cardiac angiogenesis

Project description:Purpose:The role of GDF11 in aging and cardiovascular diseases is controversial, and its function in cardiomyocytes(CMs) has not been fully explored. Methods: Total RNA was extracted from CMs using TRIzol® after CMs were transfected with shRNA-GDF11 and sh-Vector for 48h. Preparation of library and sequencing of transcriptome were carried out using Illu-mina HiSeq X Ten (Novogene Bioinformatics Technology Co., Ltd., Beijing, China). Results: Angiogenesis-related genes were the most downregulated when GDF11 was knockdown in mouse CMs. RNA-seq analysis showed that 3293 genes were downregulated and 3214 genes were upregulated when GDF11 was knockdown with shRNA-GDF11.

2023-06-01 | GSE182423 | GEO

Transcriptional profiling of GDF11 or TGFB1 stimulated NMuMG 3D spheroids

Project description:The objective of this study was to identify transcriptional changes differentially regulated by GDF11 stimulation compared to TGFB1 Microarrays were used to capture the differential transcriptional response to acute GDF11 stimulation compared to acute TGFB1 stimulation

2018-02-13 | GSE85224 | GEO

Effects of endogenous GDF11 on the odontogenic differentiation of dental pulp stem cells

Project description:Knockdown of endogenous GDF11 downregulated the odontogenic differentiation of human dental pulp stem cells (hDPSCs). We performed RNA-seq analysis on hDPSCs transfected with GDF11 small interfering RNA (siRNA) and control siRNA after 7 days of odontogenic induction, in order to investigate the underlying mechanisms of endogenous GDF11 regulating odontogenic differentiation in hDPSC.

2020-06-03 | GSE151435 | 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