Identification and characterization of enhancers for eight key arterial genes reveal transcription factors associated with different aspects of endothelial gene expression specificity and provide a tool for a better understanding of arterial differentiation.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

Single-cell multiomics reveals the gene regulatory networks and enhancer logic underlying two distinct wound response cell states in the Drosophila wing imaginal disc and finds similarities with cell states observed in the Ras-scrib tumor model.

A novel synthetic DNA cassette of CTCF-binding sites combined with the drug-controllable induction system of heterochromatin enabled switchable blocking of chromatin conformation and gene-enhancer interaction.

Silencing of gene regulatory elements by modifications of DNA-bound proteins promotes the progression of early mouse development.

Transcription-factor-dependent noncoding RNA transcription illuminates components of a transcription-factor-dependent gene regulatory network that includes enhancer-associated long noncoding RNAs and is necessary for cardiac rhythm.

Identification of activity-dependent transcriptional changes in striatal neurons reveals a conserved functional enhancer for prodynorphin.

Large-scale, allele-resolved mapping of cis-regulatory function in F₁-hybrid mice reveals sequence determinants that control transcription factor binding and enhancer activity in native chromatin context.

Pre-existing enhancers interpret T cell signaling strength in an analogue manner to direct quantitative changes in gene expression within the context of an overall digital response.

An experimental and computational system has been developed to investigate how wavelike gene expression patterns are generated during embryonic development.