Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glutamine deprivation enhances metabolic reprogramming during kidney organoid directed differentiation

ABSTRACT: Glutamine deprivation enhances metabolic reprogramming during kidney organoid directed differentiation

PROVIDER: PRJNA523040 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8588650_1.fastq.gz	Fastqsanger.gz
	SRR8588650_2.fastq.gz	Fastqsanger.gz
	SRR8588651_1.fastq.gz	Fastqsanger.gz
	SRR8588651_2.fastq.gz	Fastqsanger.gz
	SRR8588652_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Glutamine deprivation enhances directed differentiation of renal organoids

Project description:Glutamine deprivation enhances directed differentiation of renal organoids

| PRJNA529412 | ENA

Glutamine deprivation enhances metabolic reprogramming during kidney organoid directed differentiation

Project description:In this study, we systematically performed comprehensive metabolite and transcriptome profiling of human pluripotent stem cells (hPSCs) during differentiation into NPCs and later into multicellular organoids. We found activation of distinct metabolic pathways during early stage progression from hPSCs to NPCs; however, NPCs, organoids, and the intervening developmental stages between them shared similar metabolic profiles across this later stage of maturation. Importantly, the Alanine-aspartate-glutamate and glutamine pathways were significantly altered during the first stages of differentiation. Moreover, hPSCs survived glutamine deprivation during in vitro differentiation, and NPCs were successfully generated both in the absence and presence of glutamine and glutamate. Surprisingly, metabolic deprivation resulted in enhanced maturation, specifically in podocytes, as evidenced through single cell RNA-Seq analysis. These findings highlight the critical regulatory role of glutamine metabolism in the derivation of nephron progenitor cells and kidney organoids.

2025-03-20 | GSE126719 | GEO

Glutamine deprivation in U2OS cells

2014-07-31 | GSE59931 | GEO

Glutamine deprivation in U2OS cells

Project description:To understand the effects of glutamine deprivation on cell physiology we performed global analysis of gene expression in response to glutamine deprivation. U2OS cells were subjected to glutamine deprivation for 24h followed by RNA extraction and microarray analysis. U2OS cells were plated overnight followed by treatment for 24h with glutamine-containing and glutamine-depleted media. Three biological replicates were assayed for each condition.

2014-07-31 | E-GEOD-59931 | biostudies-arrayexpress

Proteomic analysis of glutamine deprivation in HepG2 cells

Project description:We applied the quantitative proteomics approach to estimate the relative abundance of proteins in HepG2 cells treated by glutamine deprivation. Two independent cultured cell lysates, namely control and glutamine deprivation, were marked with iTRAQ labels and subjected to LC-ESI-MS/MS analysis. The tryptic peptides of two samples were labeled with mass 113 (control) and 119 (glutamine deprivation) isobaric iTRAQ tags.

2016-02-09 | PXD003387 | Pride

Proteomic analysis of glutamine deprivation in HepG2 cells

2017-03-29 | MSV000080721 | MassIVE

The gene expression response of MCF7 and MDAMB231 to glutamine deprivation

Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies. Gene expression analysis in MCF7 and MDAMB231 cultured with or without glutamine for 24h

2012-01-01 | E-GEOD-26370 | biostudies-arrayexpress

The gene expression response of MCF7 and MDAMB231 to glutamine deprivation

2012-01-01 | GSE26370 | GEO

RNA sequencing analysis of A549 cells under glutamine deprivation

Project description:We performed RNA-seq ananlysis to idendity lncRNAs regulated by glutamine deprivation in A549 cells.

2024-06-29 | GSE270575 | GEO

p53 promotes cancer cell adaptation to glutamine deprivation by upregulating Slc7a3 to increase arginine uptake

Project description:Cancer cells heavily depend on the amino acid, glutamine, to meet the demands associated with growth and proliferation. Due to its rapid consumption, cancer cells frequently undergo glutamine starvation in vivo. We and others have shown that p53 is a critical regulator in metabolic stress resistance. To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation using RNA-seq analysis. We show that Slc7a3, an arginine transporter, is significantly induced by p53. We show the concomitant rise in intracellular arginine levels following glutamine deprivation is dependent on p53. The influx of arginine has minimal effect on known metabolic pathways upon glutamine deprivation. Instead, we found arginine serves as an effector for mTORC1 activation to promote in vitro and in vivo cell growth in response to glutamine starvation. Therefore, we identify a novel p53-inducible gene that contributes to the metabolic stress response.

2019-05-15 | GSE125782 | 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