The chromatin remodeler and tumor suppressor SMARCB1 acts to restrict superenhancer function to direct neural differentiation of embryonic stem cells while repressing bivalent gene activity in the pluripotent state.

A tumor-specific regulatory region has been identified upstream of the Myc oncogene.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

By focusing on RNA-binding proteins whose genes have super enhancers in smooth muscle cells, the protein RBPMS was identified as an alternative splicing master regulator.

Transcription factors of the ETS family govern a cohort of key cancer-associated regulators of malignancy in squamous cell carcinomas.

Genetic analyses reveal biological insight of a novel risk locus into systemic lupus erythematosus susceptibility.

Detailed molecular profiling investigations alongside antitumor testing and tolerability studies in animals suggest caution when considering the clinical development of inhibitors of CDK8 and CDK19, since a clear therapeutic window could not be demonstrated with two structurally distinct, potent and selective prototype drugs.

Quantitative live imaging assays reveal that multiple enhancers often fail to work in an additive fashion in the patterning of the Drosophila embryo, and sometimes even interfere with one another.

Nucleosomes at enhancers are unusually dynamic and change histone turnover rates during differentiation.

CBP/p300 acetylation of histone H3 at promoters and enhancers stimulates transcriptional elongation through recruitment of the super-elongation complex and BRD4.