The ACF chromatin-remodeling complex positions the +1 nucleosome in facultative heterochromatin to mediate transcriptional repression at Polycomb target genes.

The identification of a novel mechanism of chromatin remodeling, including a conserved remodeler domain and regulatory epitopes, provides targets for the design of therapeutics to modulate transcriptional regulation in cells.

The Chd1 motor protein performs two functionally distinct ATP-dependent activities, nucleosome assembly and chromatin remodeling, to generate periodic arrays of nucleosomes.

NODAL/Activin-induced SMAD2 binding directly drives remodeling of both open and closed chromatin and does not directly correlate with temporal patterns of gene expression upon prolonged signaling.

The unwrapping two turns of DNA on Chd1-bound nucleosomes cause the histone H3 tail and ubiquitin to be re-positioned.

Visualization of BRM remodelers engaging their endogenous genomic targets revealed highly transient and dynamic interactions with chromatin, which are fueled by ATP-hydrolysis.

Structural models of the chromatin remodeling enzyme Chd1 in solution and when bound to chromatin indicate that conformational changes to both the enzyme and the nucleosome occur upon nucleotide dependent engagement.

A technology to produce homogenously poly-ADP-ribosylated proteins reveals key molecular mechanisms that govern ATP-dependent chromatin remodeling activity at DNA damage sites.

Environmentally-mediated gene induction is extended beyond the duration of an external cue by sustaining a nucleosome-depleted chromatin structure.

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