Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cut&Run Analysis of ATF4 genomic occupancy in HCT116 colon carcinoma cell lines after treatment with DMSO, etoposide, tunicamycin, or histidinol

ABSTRACT: Cut&Run Analysis of ATF4 genomic occupancy in HCT116 colon carcinoma cell lines after treatment with DMSO, etoposide, tunicamycin, or histidinol

PROVIDER: PRJNA869708 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21060400_1.fastq.gz	Fastqsanger.gz
	SRR21060400_2.fastq.gz	Fastqsanger.gz
	SRR21060401_1.fastq.gz	Fastqsanger.gz
	SRR21060401_2.fastq.gz	Fastqsanger.gz
	SRR21060402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Cut&Run Analysis of ATF4 genomic occupancy in HCT116 colon carcinoma cell lines after treatment with DMSO, etoposide, tunicamycin, or histidinol

Project description:We examined ATF4 genomic occupancy resulting from treatment of HCT116 colon carcinoma human cell lines with DMSO, etoposide, histidinol, or, tunicamycin, using Cut&Run.

2022-08-20 | GSE211264 | GEO

RNAseq Analysis of TP53+/+ and TP53-/- HCT116 colon carcinoma cell lines after treatment with p53 or ATF4-activating compounds

Project description:We examined the gene expression changes resulting from treatment of either "wild-type" or "p53-deficient" human cell lines with compounds known to activate either p53 (nutlin-3A,etoposide) or the integrated stress response (ISR) transcription factor ATF4 (histidinol,tunicamycin)

2022-08-20 | GSE211244 | GEO

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF4 for tunicamycin treatment

Project description:To further development of our miRNA expression approach to ER stress, we have employed miRNA microarray expression profiling as a discovery platform to identify ER stress-responsible ones. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator ATF4 were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in ATF4-dependent manner were extracted. Among them, expression of three miRNAs (miR-193b, miR-423-5p, miR-199a-3p) was quantified in the RNA samples from the same as the microarray by real-time PCR. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator ATF4 were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed at each time (untreated, 12 or 24 hrs). miRNAs responsible for tunicamycin-treatment for 12hrs in ATF4-dependent manner were extracted.

2015-01-18 | E-GEOD-35175 | biostudies-arrayexpress

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF4 for tunicamycin treatment

2015-01-18 | GSE35175 | GEO

Transcriptional changes in glioma cells following treatment with 1-Benzyl-3-cetyl-2-methylimidazolium iodide (NH125), Tunicamycin, and 0.1% DMSO (in media)

Project description:Purpose: Evaluate transcriptional changes in glioma derived stem cells, U251, and normal human astrocytes following treatment with NH125, Tunicamycin, or 0.1% DMSO Methods: Glioma derived stem cells, U251 and Normal Human Astrocytes were plated in individual dishes and treated with either 2.5 micromolar NH125, 1.0 mcg/mL Tunicamycin, or 0.1% DMSO (vehicle) for twenty-four hours followed by total RNA extraction, library preparation and next generation sequencing Results: Using our analysis pipeline we mapped our sequence reads to the reference genome GRCh38. Following read count normalization and differential expression of NH125 and tunicamycin treated samples to vehicle treated controls we found that NH125 and tunicamycin treatment lead to activation of similar signalling pathways Conclusions: We present an optimized workflow for analysis of transcriptional changes in drug treated glioma derived stem cells, glioblastoma cells and normal human astrocytes

2018-03-02 | GSE102505 | GEO

ChIP-seq and mRNA-seq experiment to find the direct target genes of ATF4 and CHOP

Project description:We report the direct target genes of ATF4 and CHOP in response to endoplasim reticulum stress through next generation sequencing. By obtaining genowide sequence from chromatin immunoprecipitated DNA with anti-CHOP and anit-ATF4, we identified direct binding sites of ATF4 and CHOP in promoter regions of their target genes in mouse embrynic fibroblasts (MEFs) in response to ER stress. In addition, we obtained list of genes which are differentially regulated in Atf4 or Chop-deficient MEFs compared to the wild-type MEFs in response to ER stress. We found that genes related with unfolded protein response and protein synthesis were directly regulated by ATF4 and CHOP. Through this observation, we conclude that main role of ATF4 and CHOP as transcription factors is to enhance mRNA translation in respone to ER stress. This sutdy provide new insight of genetic network of ATF4 and CHOP in response to ER stress. For ChIP-seq, Chop+/+ and Chop-/- MEFs were treated with Tunicamycin, N-glycosylation inhibitor, to induce ER stress for 8hr. Atf4+/+ and Atf4-/- MEFs were also treated same condition for ChIP-Seq. For mRNA-seq, wild-type, Atf4-/-, and Chop-/- MEFs were treated with tunicamycin for 8hr for experiments.

2013-04-11 | E-GEOD-35681 | biostudies-arrayexpress

The mTORC1-mediated activation of ATF4 promotes protein and glutathione synthesis (Tunicamycin)

Project description:The mTORC1-mediated activation of ATF4 promotes protein and glutathione synthesis (Tunicamycin)

| PRJNA665968 | ENA

The mTORC1-mediated activation of ATF4 promotes protein and glutathione synthesis (Tunicamycin)

Project description:In response to a variety of upstream growth and oncogenic signals, the mechanistic target of rapamycin complex 1 (mTORC1) promotes anabolic metabolism, in part, through activation of downstream transcription factors. The transcription factor activating transcription factor 4 (ATF4) has been previously shown to function downstream of mTORC1 signaling to promote de novo purine synthesis and this activation of ATF4 can occur independently of the canonical activation of ATF4 through the integrated stress response (ISR). Here, we show that ATF4 activation through mTORC1 signaling drives a specific transcriptional program through ATF4 which is comprised of only a subset of genes involved in the broader cellular stress response. We find genes involved in amino acid uptake, biosynthesis, and charging by tRNA synthetases display transcriptional changes downstream of both mTORC1 and ATF4. We discovered that ATF4 activation contributes to the mTORC1-stimulated increase in protein synthesis, highlighting the importance of these transcriptional changes. Additionally, we observe regulation of the cystine transporter SLC7A11 by ATF4. We show that SLC7A11 is important for cell survival and is one mechanism by which cells with active mTORC1 signaling produce glutathione. Thus, ATF4 downstream of mTORC1 signaling regulates protein and glutathione synthesis.

2020-09-28 | GSE158605 | GEO

Development of mRNA and lincRNA expression signatures of MEFs deficient in ER stress mediators for tunicamycin treatment

Project description:To further development of our mRNA or lincRNA expression approach to ER stress, we have employed whole genome microarray expression profiling as a discovery platform to identify ER stress-responsible genes. Mouse embryonic fibroblasts (MEFs) deficient in each ER stress mediator (XBP1, ATF4, ATF6a or ATF6b) were treated with tunicamycin for 12 or 24 hrs. Genes responsible for tunicamycin in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of five ER-related genes (Derl1, Ssr3, Magt1, Bet1 and Mcfd2) was quantified in the RNA samples from COS7 cells by real-time PCR, confirming existence of similar mechanisms of trancriptional activation in ER stress by tunicamycin treatment. Mouse embryonic fibroblasts (MEFs) deficient in each ER stress mediator (XBP1, ATF4, ATF6a or ATF6b) were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed for each mediator-deficient MEF at each time (untreated, 12 or 24 hrs). Genes responsible for tunicamycin in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-01-18 | E-GEOD-35173 | biostudies-arrayexpress

Whole-genome CRISPR screen of etoposide-treated U2OS and U2OS p53KO cells, and RNAseq of U2OS cells incubated in media conditioned by etoposide-treated U2OS or U2OS p53KO cells.

Project description:CRISPR screen: U2OS or U2OS p53KO cells expressing Cas9 were transduced with a whole-genome library of CRISPR sgRNAs, then treated with either DMSO or etoposide. Differential sgRNA abundances were calculated for each condition and used to determine the effect of each single gene knockout on fitness and the drug-induced death rate. RNA-Seq: U2OS or U2OS p53KO cells were cultured with either DMSO or etoposide for 48 hours, and then U2OS cells were incubated in this conditioned media for 8 hours. RNA was collected and use to observe differential expression changes between conditions.

2023-05-17 | GSE232592 | 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