https://orcid.org/0000-0001-7051-6668
Figures & data
Figure 1. Mechanistic similarity between enhancer RNAs (eRNAs) and some enhancer-derived lncRNAs.
Diagram showing: (a) Typical eRNAs are bi-directionally transcribed from H3K4me1 marked enhancer region and may act on target promoter via chromatin looping. (b) Some lncRNAs (HOTTIP, Lockd etc.) are transcribed from H3K4me3 marked regions, and can also act on target gene promoters via chromatin looping, a mechanism identical to those performed by eRNAs/enhancers
Table 1. A list of reported eRNA binding proteins and underlying mechanisms.
Figure 2. Mechanisms underlying eRNA-RBP interaction and gene transcriptional regulation.
Several common models of eRNA-protein binding and the underlying functional mechanisms, including a) Chromatin looping, b) Regulation of the recruitment of acetylated histone reader/writer, c) Transcription factor trapping, d) Regulation of RNA Pol II Pause-release
Figure 3. A potential application of eRNA-targeting therapeutics in cancer intervention.
Diagram showing i) antisense oligo-based drug or RNAi therapeutics that can inhibit eRNAs from activating/regulating target genes; ii) small molecule compound (denoted by the dark-red pentagon object) can be developed to inhibit eRNA–protein interaction. The pink object depicts an eRNA binding protein that is involved in the oncogenic roles of the eRNA and this enhancer.
