Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

ABSTRACT: We determined if up- and/or down-regulated genes in pancreatic tumor cells cultured under low-glutamine conditions were accompanied by alterations in genome-wide chromatin accessibility and then performed ATAC-seq of KPC1199 cells treated with low glutamine concentrations versus normal-media-treated controls. The ATAC-seq was performed according to the TruePrep Tagment Enzyme for ATACseq kit (TD501, Vazyme). DNA libraries were constructed following the manufacturer’s instructions of the Trueprep index kit v2 (TD202, Vazyme) and thereafter sequenced to an average of 20 million reads per sample.

ORGANISM(S): Mus musculus

PROVIDER: GSE229051 | GEO | 2024/04/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CUT&Tag analysis of H3K36me3 and H3K27me3, in Setd2-WT and -KO murine PDAC cell line

Project description:To gain mechanistic insight into how Setd2 loss promotes activation of AKT signaling, we performed CUT&Tag sequencing in PDAC cells (KPC1199) with Setd2-KO and Setd2-WT). Setd2-WT and -KO murine PDAC cells were cultured and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K36me3 and H3K27me3 were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2023-02-06 | GSE176013 | GEO

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub and H3K27me3 in treated KPC1199 murine PDAC cell line

Project description:To gain mechanistic insight into how Epigenetic factors reprogramming tumor immune microenvironment in response to IFNγ stimulation. we performed CUT&Tag sequencing in murine PDAC cells.For comparison of the transcription profile between IFNγ-PD-L1all and IFNγ+PD-L1all cells, we treated KPC1199 cells with vehicle control or 10 ng/mL recombinant mouse IFNγ for 20 hours and harvested them. For comparison of PD-L1hi with PD-L1all, cells were either sorted with the top 15% PD-L1+ or total of IFNγ+PD-L1all PDAC cells, and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K4me3 from Abcam (ab213224), H3K27Ac from Abcam (ab4729),H2A119Ub from Cell Signaling (8240T) and H3K27me3 from Abcam (ab6002) were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2024-08-20 | GSE222133 | GEO

CUT&Tag sequencing in PDAC cells with Setd2-KO and Setd2-WT sorted from orthotopic PDAC tumor

Project description:To gain mechanistic insight into how Setd2 loss reprogramming tumor cell metabolism, we performed CUT&Tag sequencing in PDAC cells with Setd2-KO and Setd2-WT sorted from orthotopic PDAC tumor. Setd2-WT and -KO murine PDAC cells were sorted with DAPI-CD45.2-Pdpn-Epcam+ or cultured, and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K36me3, H3K27Ac and H3K27me3 were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2024-08-07 | GSE196241 | GEO

ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

Project description:ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

| PRJNA952642 | ENA

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

Glutamine deprivation in U2OS cells

2014-07-31 | GSE59931 | GEO

Autophagy is required for PDAC glutamine metabolism.

Project description:Macroautophagy (autophagy) is believed to maintain energy homeostasis by degrading unnecessary cellular components and molecules. Its implication in regulating cancer metabolism recently started to be uncovered. However, the precise roles of autophagy in cancer metabolism are still unclear. Here, we show that autophagy plays a critical role in glutamine metabolism, which is required for tumor survival. Pancreatic ductal adenocarcinoma (PDAC) cells require both autophagy and typical glutamine transporters to maintain intracellular glutamine levels. Glutamine deprivation, but not that of glucose, led to the activation of macropinocytosis-associated autophagy through TFEB induction and translocation into the nucleus. In contrast, glutamine uptake increased as a compensatory response to decreased intracellular glutamine levels upon autophagy inhibition. Moreover, autophagy inhibition and glutamine deprivation did not induce cell death, while glutamine deprivation dramatically activated apoptotic cell death upon autophagy inhibition. Interestingly, the addition of ?-ketoglutarate significantly rescued the apoptotic cell death caused by the combination of the inhibition of autophagy with glutamine deprivation. Our data suggest that macropinocytosis-associated autophagy is a critical process providing glutamine for anaplerosis of the TCA cycle in PDAC. Thus, targeting both autophagy and glutamine metabolism to completely block glutamine supply may provide new therapeutic approaches to treat refractory tumors.

| S-EPMC5124864 | biostudies-other

Single cell RNA Sequencing Analysis of Gene Expression Profile in Dgcr8 Conditional KO Embryonic Hearts

Project description:Purpose: To compare the single cell transcriptome of wild type and Mesp1Cre+/Dgcr8-/- embryonic heart at embryonic stage E9.5 Methods: For single cell sample preparation, Ventricular part of E9.5 heart tubes were dissected and digested into single cells by 0.04% Trypsin combined with 0.05% Collagenase IV, and then transferred into DMEM containing 10% fetal bovine serum for termination. After washed in PBS without Ca2+, the single cells were manually transferred into cell lysis buffer with a mouth pipette. Total RNA was reverse transcribed and amplified using Smart-seq2 protocol (Picelli et al., 2014), followed by Tn5 tagmentation and PCR enrichment to generate libraries using TruePrep DNA Library Prep Kit V2 for illumina (Vazyme, TD501-503) according to the manufacturer’s suggested protocol. Clean reads were mapped to mouse genome (mm10) using Salmon. Results: Genes significantly differentially expressed in the E9.5 Dgcr8 cKO single cardiomyocyte compared with wild type group were identified. Conclusions: Dgcr8 cKO caused important gene expression changes in E9.5 cardiomyocytes at single cell level

2018-09-12 | GSE110265 | GEO

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

Glutamine supplementation suppresses herpes simplex virus reactivation II

Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.

2017-08-30 | GSE95714 | 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