Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic analysis of glutamine deprivation in HepG2 cells

ABSTRACT: 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.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Xianghua Yan

PROVIDER: MSV000080721 | MassIVE | Wed Mar 29 00:59:00 BST 2017

SECONDARY ACCESSION(S): PXD003387

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Publications

Quantitative proteomics analysis reveals glutamine deprivation activates fatty acid β-oxidation pathway in HepG2 cells.

Long Baisheng B Muhamad Rodiallah R Yan Guokai G Yu Jie J Fan Qiwen Q Wang Zhichang Z Li Xiuzhi X Purnomoadi Agung A Achmadi Joelal J Yan Xianghua X

Amino acids 20160202 5

Glutamine, a multifunctional amino acid, functions in nutrient metabolism, energy balance, apoptosis, and cell proliferation. Lipid is an important nutrient and controls a broad range of physiological processes. Previous studies have demonstrated that glutamine can affect lipolysis and lipogenesis, but the effect of glutamine on the detailed lipid metabolism remains incompletely understood. Here, we applied the quantitative proteomics approach to estimate the relative abundance of proteins in He ...[more]

PMID: 26837383

Similar Datasets

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

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

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.

2012-01-01 | GSE26370 | GEO

The gene expression response of MCF7 and MDAMB231 to glutamine deprivation

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

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

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

Targeting Glutamine Synthetase in Tumors Disrupts Tumor Microenvironment-Regulated Cancer Cell Growth

Project description:Analysis of ovarian cancer cell line HeyA8 coculturing with cancer associated fibroblasts at gene expression level. The hypothesis test in this study is to show that cancer associated fibroblasts can influence the gene expression of HeyA8 under glutamine deprivation condition. Results provide important information of the response of HeyA8 when coculturing with cancer associated fibroblasts under glutamine deprivation, such as cell proliferation, apoptosis

2016-10-09 | GSE87773 | GEO

Glutamine deprivation enhances directed differentiation of renal organoids

Project description:Glutamine deprivation enhances directed differentiation of renal organoids

| PRJNA529412 | ENA

Phosphoethanolamine Accumulation Protects Cancer Cells under Glutamine Starvation through Downregulation of PCYT2

Project description:The conditions of the tumor microenvironment, such as nutrient starvation, play critical roles in cancer progression. However, the role of glutamine deprivation in cancer progression is not studied as extensively as that of hypoxia. Here, we show that glutamine starvation triggered down-regulation of PCYT2 by stimulating accumulation of PEtn. Interestingly, glutamine upregulated series of glutamine-responsive genes, not only PCYT2. Furthermore, glutamine-responsive genes were associated with overall survival of cancer patients. Thus, our findings show that glutamine responsive genes such as PCYT2 are key for progression of cancer cells, partly protecting cancer cells to glutamine starvation.

2019-08-24 | GSE136289 | 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