An increasing body of evidence suggests that SEs play a crucial role in tumor growth and that oncogenic SEs induce oncogene transcription and continually increase cell survival and proliferation, implying that inhibiting SEs is a viable anticancer treatment [215]. However, it is challenging to use S...
For example, transcription across the yeast SER3 promoter interferes with the binding of activators, resulting in gene repression[21]. Another illustration from the yeasts is the dislodging of Rap1 and Gcr1 factors from the ADH1 promoter by non-coding intergenic RNA ZRR1[22]. In order to ...
Super-enhancers (SEs) consist of multiple typical enhancers enriched at high density with transcription factors, histone-modifying enzymes and cofactors. Oncogenic SEs promote tumorigenesis and malignancy by altering protein-coding gene expression and noncoding regulatory element function. Therefore, they pla...
histone modification and act as scaffolds for recruitment of additional factors. These cofactors include, but are not limited to, SWI/SNF and FACT chromatin remodelling complexes, P300 and CBP chromatin activators, Bromodomain-containing (BRD)
Enhancers were originally identified as long-range activators of gene transcription in higher eukaryotes and they were the first DNA sequences found to confer tissue specificity. These properties had set them apart from previously described upstream promoter elements of eukaryotic genes. More recent inves...
Transcriptional enhancers are regulatory DNAs that instruct when and where genes should be transcribed in response to a variety of intrinsic and external signals. They contain a cluster of binding sites for sequence‐specific transcription factors and co‐activators to determine the spatiotemporal ...
They can be bound with proteins (activators) to activate transcription of a gene, and hence play a critical role in promoting gene transcription in eukaryotes. With the avalanche of DNA sequences generated in the post-genomic age, it is a challenging task to develop computational methods for ...
in a poised state (Fig.1C). In an active state, enhancers are enriched with both the activating H3K27ac and H3K4me1 modifications, facilitating the binding of TFs and co-activators (Fig.1D). This interaction establishes enhancer-promoter (E-P) loops, thereby driving transcription [16,19,...
For example, the rescue of A-485-induced transcription inhibition by TSA suggests that a diminished KDAC activity (i.e., caused by a genetic mutation in KDACs or their activators) could lead to a resistance to p300/CBP inhibitors. However, because p300/CBP activity promotes RNAPII recruitment...
(e.g. CBP/P300 and HDAC), transcriptional co-activators (e.g. MED1 and BRD4) and RNA polymerase II (RNA pol II) [33,34,35]. However, it is unclear how SEs recruit these transcriptional regulators. Here, we briefly describe the process by which SEs form transcription complexes stepwise...