2023年3月8日 · IGV browser shows ChIP-seq signal tracks for CTCF, SMC1, RelA, H3K27ac. The location of super-enhancers (SE), if any, were shown under H3K27ac ChIP-seq signal tracks.

2020年1月7日 · We analysed CTCF ChIP-seq data for normal prostate cells (PrEC) and prostate cancer cell line (LNCaP) 16 and found that the CTCF-binding pattern was strikingly similar across the locus...

2020年11月5日 · Combining cohesin ChIP-seq and single-molecule imaging in live cells, we observe that although CTCF localizes cohesin at its binding sites, it does not control overall binding or dynamics of...

Systematic chromatin immunoprecipitation experiments combined with high-throughput sequencing (ChIP-seq) have been performed to map CTCF binding events across the genome in many tissues of different species [8 – 10]. They show that the genome is covered with a myriad of CTCF binding sites.

2020年5月11日 · We first performed ChIP-seq (by ChIPmentation) to examine how DNA binding of transgenic CTCF or CTCFL changes in the presence (D) and absence (ID) of endogenous CTCF, using the FLAG tag in the transgenes.

2022年4月5日 · To understand the regulatory mechanism of CTCF on reprogramming, we performed CTCF chromatin immunoprecipitation (ChIP)-seq experiments on different reprogramming intermediates reprogrammed by OSKM with or without Ctcf knockdown (Figure 2 …

2020年9月23日 · To study the evolution of CTCF binding between closely related species, we performed chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) in liver samples from two mouse subspecies: BL6 and CAST ( Methods ).

2022年12月16日 · CTCF binds DNA through the combinatorial use of its 11-zinc-finger domains to target sites with remarkable sequence variation (Jolma et al., 2013; Ohlsson et al., 2001). A 15–20 bp CTCF consensus motif from the ChIP-seq data analysis has been defined (Kim et al., 2007), referred to hereafter as M1. This motif interacts with the central zinc ...

2023年10月31日 · The binding motifs for myogenic regulatory factors, including Myf5, MyoD, and MyoG, were enriched in muscle-cell-specific CBSs. The colocalization of CTCF and lineage-specific TFs around the lineage-specific CBSs was supported by ChIP-seq signal analysis (Figures 1C and 1F).

To test whether CTCF causes local RNAPII stalling, we examined PRO-seq signals at the CBSs following CTCF degradation. Surprisingly, we found stalling at the CBSs remains fully intact despite ChIP-seq-validated loss of CTCF binding (Figures 3C, 3D, and S3F).