Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA175811 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR575707.fastq.gz | Fastqsanger.gz | |||
| SRR575708.fastq.gz | Fastqsanger.gz | |||
| SRR575709.fastq.gz | Fastqsanger.gz | |||
| SRR575710.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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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.
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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.
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Project description:Global identification of activated GR and p65 binding sites and target genes using ChIP-seq in HeLa B2 cells. generation genome-wide chromatin state-maps of GR, p65 and RNAPII in HeLa B2 cells under conditions 1) DMSO (control); 2) TA 1M-BM-5M 4hr; 3) TNFM-NM-1 10ng/ml ; 4) TA 1M-BM-5M 4hr at at third hour 10ng/ml TNF M-NM-1 was added
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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.
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