In addition, see/read about BORIS-driven reprogramming of 3D Chromatin Looping including physical Enhancer-Promoter communication in the following Nature paper: https://t.co/3NMML8QkyL https://t.co/YTbO2nHemk
Indeed, aberrant activation of CTCF Like BORIS in the widely utilized K562 (and other cancer cells) results in switching Promoter-specific Enhancer Loops from CTCF-only-bound anchors to CTCF & BORIS co-bound Pol2+ anchors, shown in Fig S11 reproduced b
There is an inherent structure-functional dichotomy between double and single CTCF sites unresolvable by ChIP-Seq alone Promoter-Enhancer pairs bound by RNAPII and marked by H3K27-acetylation are depleted in single but enriched in double CTCF sites http
In addition, in accord w/ original discovery of double CTCF sites unresolvable by CTCF ChIP-Seq alone https://t.co/XE950LxSWX, BORIS binds to specific sites encompassing at least 2 adjacent CTCF binding DNA motifs recognized by multivalent 11ZF DBD shared