Single-molecule imaging of CTCF and cohesin in live cells suggests that chromatin loops are dynamic structures that frequently form and fall apart.

Absolute quantification of CTCF and cohesin reveals quantitative constraints on 3D genome organization and illuminates the molecular architecture of the cohesin complex.

In contrast to other transcription factors, CTCF and Esrrb rapidly regain binding after replication and remain bound to their targets during mitosis, preserving local nucleosome organization throughout the cell cycle.

CTCF protects cohesin^STAG1 from WAPL.

Absolute quantification of cohesin, CTCF, NIPBL, WAPL and sororin in HeLa cells implies that some genomic cohesin and CTCF enrichment sites are unoccupied at any one time.

Certain types of 3D chromatin loops are easy to predict from existing or easily obtainable 2D information, which benefits gene expression studies in tissues/cells/organisms without extensive pre-existing 3D information.

The chromosome architectural protein, CTCF, is phosphorylated at Ser²²⁴ in a cell-cycle-dependent manner and abrogation of phosphorylation leads to a cell growth defect.

Though generally considered a transcriptional repressor, Wiz may also function as a transcriptional activator in the mouse brain and is required for normal behaviour.

The 3'HS1 CTCF binding site directly modulates chromosomal loops to regulate γ-globin expression through the accession of the hereditary persistence of fetal hemoglobin enhancer.

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.