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Journal ArticleDOI

Subset of genes targeted by transcription factor NF-κB in TNFα-stimulated human HeLa cells

Yujun Xing, +2 more
- 01 Mar 2013 - 
- Vol. 13, Iss: 1, pp 143-154
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TLDR
The direct target genes (DTGs) of NF-κB in the TNFα-stimulated HeLa cells were identify by using ChIP-Seq, RNAi, and gene expression profiling techniques, and it was revealed that 50 % of these genes contained canonical κB sites in their ChIP peaks and 90 % contained non-canonical κBs in theirChIP peaks.
Abstract
Nuclear factor κB (NF-κB) is a ubiquitous transcription factor that plays a pivotal role in controlling important cellular processes, ranging from normal cell growth and differentiation to apoptosis and cancer. In recent years, many new target genes of NF-κB have been identified in several cell lines that were treated with various stimuli using chromatin immunoprecipitation (ChIP)-based high-throughput techniques. However, the target genes from various cell lines and stimuli are not identical, and many of them are cell or stimulus specific. This suggests that it is necessary to investigate different cell lines and stimuli for identifying all target genes of this transcription factor. In this study, the direct target genes (DTGs) of NF-κB in the TNFα-stimulated HeLa cells were identify by using ChIP-Seq, RNAi, and gene expression profiling techniques. As a result, 584 DTGs were identified, in which 266 were activated and 318 were repressed. The κB motif searching revealed that 50 % of these genes contained canonical κB sites in their ChIP peaks and 90 % contained non-canonical κB sites in their ChIP peaks. In comparison with target genes identified in LPS-treated U937 and THP-1, only limited numbers (10∼23) of target genes were shared by each of two cell lines, and only two gene (NFKB2 and STAT5A) were commonly shared by three cell lines.

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Citations
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The Toxoplasma effector TEEGR promotes parasite persistence by modulating NF-κB signalling via EZH2

TL;DR: Following export from the parasite, the dense granule-resident effector TEEGR travels to the host cell nucleus where it interferes with host transcription factors to modulate immune signalling and regulate Toxoplasma persistence.
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Detection of regulatory SNPs in human genome using ChIP-seq ENCODE data.

TL;DR: An approach aggregating the whole set of ENCODE ChIP-seq data in order to search for rSNPs is described, and experimental evidence of its efficiency is provided, based on the assumption that the enrichment of a genomic region with transcription factor binding loci indicates its regulatory function and thereby SNPs located in this region are more likely to influence transcription regulation.
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NF-κB target microRNAs and their target genes in TNFα-stimulated HeLa Cells

TL;DR: The expression of miR-125b-1 regulated by NF-κB has been reported in diverse cell types under various stimuli, and this study found that its expression was also significantly regulated byNF-κBs in TNFα-stimulated HeLa and HepG2 cells, suggesting that this little known miRNA might play roles in these diseases via its two target genes of BMP2 and CASP9.
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C26 cancer-induced muscle wasting is IKKβ-dependent and NF-kappaB-independent.

TL;DR: The data support the idea that although inhibition of IκBα, and particularly IKKβ, blocks cancer-induced wasting, the alternative NF-κB signaling pathway is not required, and the downstream NF-kkB transcription factors, p65 and c-Rel do not appear to regulate the transcriptional changes induced by the C26 tumor.
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Characterization of genome-wide binding of NF-κB in TNFα-stimulated HeLa cells

TL;DR: In vivo genome-wide binding characteristics of NF-κB RelA exerted effects on the transcription of its direct target genes in genome, reflecting some important traits of this protein which acts as a stimulatory transcription factor involving in many biological processes and responding to various internal and external stimuli.
References
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