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Acetylation of p65 at lysine 314 is important for late NF-k(kappa)B-dependent gene expression

ABSTRACT: We provided earlier evidence that acetylation of p65 at lysines 310, 314 and 315 is important for the expression of a defined subset of genes; acetylation at these residues regulates both positively and negatively gene expression, in a gene-specific manner. These earlier studies provided a first glance of the functional relevance of p65 acetylation, since gene expression was measured only after 45 minutes of TNFα stimulation. In order to know if the requirement for site-specific acetylation is maintained for the same genes after longer exposure to TNFα, and to identify possible new genes regulated through p65 acetylation, we decided to extent our analysis to 3 hours of stimulation. For this, we used p65(-/-) MEFs complemented with non-acetylatable mutants, where the target lysines for acetylation were mutated to arginines.

ORGANISM(S): Mus musculus

PROVIDER: GSE15196 | GEO | 2010/01/10

SECONDARY ACCESSION(S): PRJNA116417

REPOSITORIES: GEO

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Acetylation of p65 at lysine 314 is important for late NF-k(kappa)B-dependent gene expression

Project description:We provided earlier evidence that acetylation of p65 at lysines 310, 314 and 315 is important for the expression of a defined subset of genes; acetylation at these residues regulates both positively and negatively gene expression, in a gene-specific manner. These earlier studies provided a first glance of the functional relevance of p65 acetylation, since gene expression was measured only after 45 minutes of TNFÎ± stimulation. In order to know if the requirement for site-specific acetylation is maintained for the same genes after longer exposure to TNFÎ±, and to identify possible new genes regulated through p65 acetylation, we decided to extent our analysis to 3 hours of stimulation. For this, we used p65(-/-) MEFs complemented with non-acetylatable mutants, where the target lysines for acetylation were mutated to arginines. p65(-/-) cells complemented either with wild type p65, an empty plasmid as control (pTV), the acetylation-deficient double mutant K314/315R or the triple mutant KTR (K310/314/315R), were stimulated by TNFÎ± for 3 hours and total RNA was isolated in three independent replicates from these cells. RNA was amplified, labeled and hybridized to the Agilent Whole Mouse Genome Array. After statistical analysis of the expression profiles, differentially expressed genes were identified.

2010-04-08 | E-GEOD-15196 | biostudies-arrayexpress

Genome-wide TNFα-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFα-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFα-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFα treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFα stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli.

2012-11-26 | GSE41100 | GEO

RNA-seq analysis from epididymis and testis of ArKI mice

Project description:We generated a mouse model (ArKI) in which the two conserved SUMO acceptor lysines of androgen receptor (AR) were permanently abolished by converting them to arginines (ArK381R, K500R). RNA-seq was used to analyse how the lack of AR SUMOylation affects the gene expression pattern of selected tissues.

2019-01-09 | GSE112697 | GEO

ChIP-seq analysis of androgen receptor binding in epididymis of ArKI mice

Project description:To analyze how SUMOylation of AR affects its chromatin binding, we generated a mouse model (ArKI) in which the two conserved SUMO acceptor lysines of androgen receptor (AR) were permanently abolished by converting them to arginines (ArK381R, K500R). ChIP-seq was used to analyse how the lack of AR SUMOylation affects the chromatin binding of AR in epididymis.

2019-01-09 | GSE121151 | GEO

Genome-wide BRD4, PolII and p65 occupancy as well as chromatin modifications in bone marrow derived macrophages from BRD4 conditional KO mice

Project description:We are reporting here genome wide distribution of BRD4 in bone marrow derived macrophages at steady state level and in reponse to LPS stimulation. In both condition, BRD4 distribution was found to be widespread in intragenic as well as intergenic regions with enrichment specifically near TSS. Characteristically BRD4 signal were highly enriched on enhancers of some active genes and hence were classified as BRD4 rich super-enhancers (>12kb long stretches). Super-enhancers are formed, in some instances by redistribution of BRD4 on LPS stimulated genes. BRD4 binding well correlated PolII binding at the chromatin acetylated at H3K27, H3K9 and H4tetraK. Interestingly many LPS induced BRD4 independent genes, despite BRD4 loss in the KO, maintained PolII binding at the chromatin enriched with acetylated lysines at H3K27, H3K9 and H4tetraK. Additionally among some BRD4 independent LPS inducible genes we detected stronger p65 enrichment in the KO. In contrast, P65 binding was not detected in BRD4 dependent genes. These observations provided evidence of plasticity of epigenetic changes in retaining inflammatory reponses in macrophages.

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Project description:Inflammation is involved in both initiation and promotion of colorectal cancer (CRC), and patients with inflammatory bowel disease (IBC) have increased risk of developing CRC. Tumor necrosis factor alpha (TNFα) is a cytokine secreted by e.g. macrophages, and this signaling is deregulated in IBD and CRC. TNFα activates the pro-survival transcription factor complex NFκB, which is composed of several subunits including p65 (RELA). We recently characterized the genome-wide transcriptional impact by TNFα in two CRC cell lines, but how p65 binds the chromatin, its cistrome, in colorectal cancer cells has not been explored. We here used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in HT29 and SW480 cells, and correlated with the transcriptomic impact of TNFα. Further, estrogen receptor beta (ERβ) has anti-inflammatory and anti-tumorigenic effects in colon cells and interacts with NFκB main targets. We have shown that ERβ impacts TNFα signaling in CRC cells and ERβ impacts the P65 cistrome.

2021-03-01 | GSE160856 | GEO

A2M-3K DSSO cross-linking to identify the bait region position

Project description:An A2M mutant, A2M-3K, with the bait region arginines replaced with lysines, was cross-linked with DSSO. Its monomeric gel band was analyzed by XL-MS to identify the bait region position within a subunit.

2021-05-21 | PXD019048 | Pride

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells II

Project description:Chronic inflammation promotes cancer progression by affecting the tumor cells and their microenvironment. Here, we demonstrate that the continuous stimulation (6 weeks) of triple-negative breast tumor cells (TNBC) by the potent pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) had a robust effect on gene expression, demonstrating that the cancer cells have been skewed to strong pro-inflammatory phenotype. Moreover, continuous TNFα + IL-1β stimulation has reduced cell-to-cell contacts in the cancer cells and has induced metabolic plasticity in TNBC cells: this was exemplified by increase in active mitochondria area and elevations in the glycolytic as well as mitochondrial respiratory potential of the cancer cells (OXPHOS). Glycolysis has induced p65 activation and has led to increased transcription and expression of pro-metastatic chemokines such as CXCL8, CXCL1 and CCL2 and sICAM-1; agreeing with the ability of these chemokines to induce the recruitment of deleterious myeloid cells to tumors, mainly inhibition of glycolysis has given rise to reduced monocytic cell migration, in vitro and in vivo, in response to cancer cell supernatants obtained following continuous TNFα + IL-1β stimulation. Such inflammation-induced metabolic plasticity, which promotes metastatic cascades in TNBC, may have important clinical implications in the treatment of TNBC patients

2021-05-30 | GSE169017 | GEO

Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells I

2021-05-30 | GSE169016 | GEO

Transcriptome analysis of IEC4.1 cells in response to TNFα stimulation.

Project description:Mouse intestinal epithelial cells (IEC4.1 cells) were stimulated with TNFα (10 ng/ml) for 4h. The Agilent SurePrint G3 Mouse Gene Expression Microarray (G4852A) was used for the analysis, which provides full coverage of genes and transcripts with the most up-to-date content, including mRNAs and lincRNAs (http://www.chem.agilent.com/store/en_US/Prod-G4852A/G4852A). IEC4.1 cells were grown to 80% confluence for four groups: the siRNA control (Group A, cells treated with a non-specific scrambied siRNA control), the TNFα -stimulated (Group B, cells treated with the siRNA control plus TNFα stimulation), lincRNA-Cox2 siRNA (Group C, cells treated with an siRNA to lincRNA-Cox2), and lincRNA-Cox2 siRNA/ TNFα stimulated (Group D, cells treated with the lincNRA-Cox2 siRNA plus TNFα stimulation). Cells were treated with the siRNAs for 24h, followed by additional culture for 4h in the presence or absence of TNFα (10 ng/ml). Total RNAs were prepared with the RNeasy Mini kit (Qiagen) according to the manufacturer’s instruction (Ambion).

2016-10-25 | E-MTAB-3904 | biostudies-arrayexpress

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