Combinatorial transcription factor binding shared by multiple species enriches for essential biological pathways and coincides with disease-causing regulatory DNA mutations.

A large-scale transcription factor screen reveals over twenty novel adipogenic regulators: most notably ZEB1, which exerts essential transcriptional control of fat cell differentiation.

A pooled mutational scanning approach for 3D chromosome conformation reveals how multiple transcription factors can jointly specify condition-specific genome conformations.

Drosophila has almost all transcription factor binding specificities available to humans; and human transcription factors with divergent specificities operate in cell types that are not found in fruit flies.

Confronting different models of chromatin accessibility with temporally resolved transcription profiles favors a scenario where transcription factors actively, rather than passively, drive chromatin from the inaccessible to the accessible state.

Making human stem cells express certain transcription factors can convert them into cells that are similar to ovarian granulosa cells, and perform several important functions of the ovary.

Protein binding microarrays highlight the diversification of DNA-binding motifs for the nuclear hormone receptor and C2H2 zinc finger transcription factor families, and reveal unexpected diversity in motifs for the T-box and DM families.

Spatial factors generate neuroblast-specific open chromatin, thereby biasing the subsequent binding of transcription factors to produce neuroblast-specific neurons.

The epistasis observed in TF-DNA binding preferences can be explained by the presence of two optima of very similar Gibbs energy that are located relatively far from each other in sequence space.

Collaborative transcription factors (TFs) exhibit a dominant pattern of a relaxed range of spacing and substantial tolerance of spacing alterations resulting from naturally occurring insertions and deletions in comparison to genetic variants directly affecting TF binding sites.