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Genome-wide RELA binding sites in response to 5 microbial stimuli in Detroit562 cells [ChIP-seq]

ABSTRACT: NFKB is a family of transcription factors (TF), which are master regulators of the innate immune system. It is activated downstream of pathogen recognition receptors after ligand binding and regulates the expression of antimicrobials, cytokines and chemokines, thus helping to fight infections as well as recruiting the adaptive immune system. Although NFKB responds to a wide variety of signals, the processes in which stimulus-specificity is attained are still unclear. Here, we characterized the response of one of the NFKB members, RELA, to five stimuli mimicking infection in nasopharyngeal epithelial cells. When comparing RELA genome-wide binding sites , we detected most of them to be overlapping among the different stimulations. Yet, we distinguished a minority of stimulus-specific RELA binding sites. Interestingly, some of these seemed to have a biological effect as they correlated with corresponding gene expression. Specifically, the response to Poly I:C mimicking viral dsRNA gave a distinct RELA profile binding the vicinity of antiviral genes. This group of binding sites was also enriched in Interferon Regulatory Factor motifs indicating that the interaction with more specialized TFs could contribute to stimulus-specific RELA activity. Furthermore, motif analysis revealed differences in the sequence of the NFKB motifs between certain stimulus-specific sets of peaks suggesting preferences for particular NFKB dimers in response to defined signals.

ORGANISM(S): Homo sapiens

PROVIDER: GSE91018 | GEO | 2018/01/30

REPOSITORIES: GEO

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