GSE41100
Genome-wide TNFa-induced p65 binding before and after telomerase inhibition in HeLa cells
Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFa-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFa-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFa treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFa 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. Overall design: Examination of p65 binding in HeLa cells in absence and presence of TNFa and MST-312.