Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18186300_1.fastq.gz | Fastqsanger.gz | |||
| SRR18186300_2.fastq.gz | Fastqsanger.gz | |||
| SRR18186301_1.fastq.gz | Fastqsanger.gz | |||
| SRR18186301_2.fastq.gz | Fastqsanger.gz | |||
| SRR18186302_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFM-NM-1-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFM-NM-1-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFM-NM-1 treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFM-NM-1 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. Examination of p65 binding in HeLa cells in absence and presence of TNFM-NM-1 and MST-312.
2012-11-26 | E-GEOD-41100 | biostudies-arrayexpress
Project description:In effort to develop methodology for targeted top down mass spectrometry of NF kappa B p65 from human cells, we evaluated the utility of HaloTag for purification and analysis of recombinant protein. During our study, two datasets of bottom up LC-MS/MS were generated: one from in-gel digestion of the predominant band following p65-HaloTag purification, another from in-solution digestion of all the proteins present in a p65-HaloTag purification. p65-HaloTag copurifying proteins identified in our datasets include the known interactors c-Rel, NF-kappaB p105, NF-kappaB p100, and NF-kappaB inhibitor beta. Over 100 proteins were identified by at least two peptides using a Mascot ion cut-off score of 30.
2018-10-19 | PXD001932 | Pride
Project description:We look at differential gene expression between immortalized p65+/+ and p65-/- MEFs to identify potential NF-kB regulated genes which when grouped based on biological function indicates candidates involved in protecting p65+/+ cells from macrophage-mediated killing
2017-10-01 | GSE101092 | GEO
Project description:We investigated the ability of the NFkB protein p65 to bind DNA after RNA digestion. In this ChIP-seq experiment, we investigated the genome-wide binding profiles of p65 in Jurkat cells. We demonstrated that p65 binding to promoters and promoter proximal regions is enhanced by digestion of RNA with RNase A.
2022-03-08 | GSE197704 | GEO
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
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
Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-κB subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-κB p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-κB-dependent enhancers in epithelial cells. ChIP-seq in KB cells with 5 different antibodies under different treatment conditions
2014-12-16 | E-GEOD-64223 | biostudies-arrayexpress
Project description:TNF alpha is one of the inflammatory mediator and induce genes mainly by transcriptional factor, p65, in endothelial cells. This time, we performed a time course study to detect the change of localization of p65 and Pol II. To identify p65 and Pol II binding sites, we used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without TNF alpha for 30 mins. Cells were starved before stimulation longer than 16 hours. HUVECs were used within the first 6 passages. For crosslinking, 10 mM of EGS in 50% glacial acetic acid was used for 45 min, followed by 20 min of 1% paraformaldehyde treatmet was used.
2013-01-01 | E-GEOD-34500 | biostudies-arrayexpress
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).
2012-03-31 | E-GEOD-36568 | biostudies-arrayexpress
Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).
2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress