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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33990 | GEO | 2012/05/31

SECONDARY ACCESSION(S): PRJNA150633

REPOSITORIES: GEO

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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. 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.

2012-05-30 | E-GEOD-33990 | biostudies-arrayexpress

Temporal modulation of the NF-kB network in response to different types of DNA damage ETOPOSIDE C4PR_LIV

Project description:Different types of DNA damage can initiate phosphorylation-mediated signalling cascades that result in stimulus specific pro- or anti-apoptotic cellular responses. Amongst its many roles, the NF-κB transcription factor RelA is central to the DNA damage response pathway. Yet, understanding of the co-ordinated signalling mechanisms that result in these different DNA damaging agents inducing specific cellular outcomes through RelA remains unclear. Here, we examine the temporal effects of exposure of U2OS cells to either etoposide (ETO) or hydroxyurea (HU) on the phosphorylation status of RelA and its protein binding partners, using label-free quantitative phosphoproteomics. Although there were relatively few stimulus specific differences overall in the phosphorylated RelA interactome in response to either DNA damaging agent, we observed subtle, but significant changes in the phosphorylation states of the RelA bound proteins as a function of both the type of and duration of the DNA damaging agent used. The DNA double strand break (DSB) inducing ETO invoked more rapid, sustained responses than HU, with regulated targets primarily involved in transcription, cell division and (unsurprisingly) DSB repair. Kinase substrate prediction of confident, differentially regulated phosphosites suggests possible roles for CDK1 and MAPK3/ERK1 signaling, in addition to the known roles of ATM/ATR. In contrast, HU-induced replicative stress mediated more temporally dynamic regulation, with phosphoprotein components of the RelA network having known roles in rRNA/mRNA processing and translational initiation, many of which contained a 14-3-3ε binding motif. Our data thus point to differential regulation of key cellular processes and the involvement of unique signalling pathways in modulating DNA damage-specific functions of RelA.

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Myeloid cell RelA/p65 promotes lung cancer proliferation

Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).

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Myeloid cell RelA/p65 promotes lung cancer proliferation

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Transcriptome profiling of murine overexpression of p65/RelA mutants III

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

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Project description:p65

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Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Project description:Using a mouse model with hepatocyte-specific deletion of transcription factor NF-κB RelA (p65), our group has previously revealed the important role of RelA in inducing the acute phase response, maintaining host defense, and preventing liver injury during sepsis. To goal of this study was determine the influence of RelA on hepatic gene changes that provide liver protection during infection. Mice were generated with functional deletion of NF-kappaB RelA (p56) in hepatocytes using a Cre-LoxP system. Mutant mice expressed Cre-recombinase under the transcriptional control of an albumin promotor and homozygous floxed RelA alleles. Wild type control mice lack the Cre-recombinase. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal bacteremia.

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Project description:MTSS1 Suppresses NF-kB Activity in Lung Adenocarcinoma through Repression of RelA/p65 Phosphorylation

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