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Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Cell imaging and mathematical modelling show reciprocal cross-regulation between inflammatory signalling and cell cycle timing, which is mediated through functional interactions between NF-B and E2F proteins.

The Hox transcription factor Ultrabithorax (Ubx) represses alternative gene programs during lineage development by lineage-specific Polycomb protein complex retention at Ubx-targeted chromatin sites.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

The transcription factor Snai1b maintains the myocardial wall integrity by limiting cell extrusions and regulating the intermediate filament gene desmin b.

Transcription factor proteins play an important role in modulating base damage formation and excision repair at the binding sites in the genome.

Maternally deposited Piwi-piRNA complexes co-transcriptionally repress transposable elements that transiently become active in somatic cells of the developing Drosophila embryo.

Replication origins are established throughout the genome with the exception of transcribed genes, and the local chromatin composition likely modulates the density of ORC and MCM as well as origin activation.

An integrative genome-wide approach supports a direct and collaborative role of ETS and AP-1 transcription factors in maintaining endothelial cell-specific and anti-inflammatory gene expression programs.

A genome scale model of Brugia malayi metabolism illustrates a dynamic reliance on energy production pathways across its life cycle and identifies new drugs with experimentally supported anti-parasitic properties.