Department of Pathology, NYU Grossman School of Medicine, New York, NY, USA; Perlmutter Cancer Center, NYU Langone Health, New York, NY, USA.
Department of Pathology, NYU Grossman School of Medicine, New York, NY, USA; Perlmutter Cancer Center, NYU Langone Health, New York, NY, USA. Electronic address: https://twitter.com/@Ryo2Iwata.
Curr Opin Genet Dev. 2024 Oct;88:102244. doi: 10.1016/j.gde.2024.102244. Epub 2024 Aug 13.
A number of factors contribute to cell type-specific CTCF chromatin binding, but how they act in concert to determine binding stability and functionality has not been fully elucidated. In this review, we tie together different layers of regulation to provide a holistic view of what is known. What emerges from these studies is a multifaceted system in which DNA sequence, DNA and chromatin accessibility, and cell type-specific transcription factors together contribute to CTCF binding profile and function. We discuss these findings in the light of disease settings in which changes in the chromatin landscape and transcriptional programming can disrupt CTCF's binding profile and involvement in looping.
许多因素导致了细胞类型特异性 CTCF 染色质结合,但它们如何协同作用以确定结合的稳定性和功能尚未完全阐明。在这篇综述中,我们将不同层次的调控联系起来,提供一个全面的视角。从这些研究中可以看出,一个多方面的系统,其中 DNA 序列、DNA 和染色质可及性以及细胞类型特异性转录因子共同促成了 CTCF 结合谱和功能。我们将根据染色质景观和转录编程变化可破坏 CTCF 结合谱及其在环化中的参与的疾病情况来讨论这些发现。