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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptomic analysis of Etoposide-treated 293 cells expressing p65 wt or p65 S547A

ABSTRACT: We reported a direct phosphorylation of the Ser547 of the RelA/p65 subunit of NF-kB by ATM kinase. A comparative transcriptomic analyse with HEK293 cells expressing exclusively HA-p65wt or a non-phosphorylable mutant HA-p65S547A was conducted to identify the genes regulated by this phosphorylation after an Etoposide treatment. HEK293 cells expressing exclusively HA-p65wt or HA-p65S547A were treated during four or eight hours with Etoposide or left untreated. This was performed three times to obtain independent triplicates for the microarray expermiment.

ORGANISM(S): Homo sapiens

SUBMITTER: Helene Sabatel

PROVIDER: E-GEOD-33990 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptomic analysis of Etoposide-treated 293 cells expressing p65 wt or p65 S547A

Project description:We reported a direct phosphorylation of the Ser547 of the RelA/p65 subunit of NF-kB by ATM kinase. A comparative transcriptomic analyse with HEK293 cells expressing exclusively HA-p65wt or a non-phosphorylable mutant HA-p65S547A was conducted to identify the genes regulated by this phosphorylation after an Etoposide treatment.

2012-05-31 | GSE33990 | GEO

Comparative phosphoproteomic analysis of HeLa cells in response to etoposide or to a combination of etoposide and the ATR inhibitor VE821

Project description:To investigate the regulation of protein phosphorylation during the DNA damage response and the role of ATR kinase activity, we performed a comparative phosphoproteomic analysis of HeLa cells treated with etoposide alone or in combination with the ATR inhibitor VE821. Etoposide is a topoisomerase II inhibitor that induces DNA double-strand breaks, activating the DNA damage signaling cascade. We focused particularly on phosphorylation events associated with Treacle (TCOF1), a nucleolar protein implicated in the regulation of rDNA transcription and nucleolar DNA damage response. Quantitative mass spectrometry-based phosphoproteomics was used to identify and quantify global phosphorylation changes under both treatment conditions. This dataset enables the identification of ATR-dependent phosphorylation sites and may provide insights into the molecular mechanisms underlying nucleolar stress responses and the coordination of DNA repair processes.

2026-05-25 | PXD067042 | Pride

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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.

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RNA-seq of sh2-H2AFJ and sh-NoTarget in WI-38hTERT cells induced into senescence by etoposide

Project description:Study the role of H2A.J in gene expression in senescent human fibroblasts by comparing RNA-seq of WI-38hTERT fibroblasts expressing either an sh2-H2AFJ or sh-NoTarget RNAs. Senescence was induced by treating cells with 20 M etoposide for 2 weeks followed by one further week of incubation without etoposide. 3 biological replicates of sh2-H2AFJ and sh-NoTarget were sequenced.

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Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-Seq]

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Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-chip]

2012-05-03 | GSE36751 | GEO

AP-MS of GFP-MCM2 in the cellular response to etoposide induced DNA damage.

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2017-08-14 | GSE99028 | GEO

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Project description:To study the senescence gene signatures in the cells, which were genetic SMARCB1 depleted or treated with aurora kinase inhibitors or etoposide, we performed next generation RNA sequencing on these cell, and 'FRIDMAN_SENESCENCE_UP' geneset was used to determine the enrichment of senescence-related genes. The RNA sequencing results include (1) A375 cells and SMARCB1 depleted counterparts. (2) A549 cells and aurora kinase inhibitor (Alisertib, barasertib or tozasertib) or etoposide treated counterparts.

2017-09-21 | GSE102639 | GEO

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