Eun-Chong Lee
Yonsei University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Eun-Chong Lee's research lab focuses on the role of chromatin architecture, particularly CTCF-mediated genome organization, in regulating gene expression across immune cells and metabolic tissues. The lab investigates how three-dimensional genome dynamics—such as chromatin looping, phase-separated transcriptional condensates, and enhancer-promoter interactions—govern cell identity, immune responses, and metabolic homeostasis. Using integrative multi-omics approaches, including 3C-based methods, single-cell genomics, and epigenomic profiling, the lab uncovers the mechanistic links between 3D genome organization and disease-relevant gene regulation. Their work reveals how disruptions in CTCF function lead to immune dysregulation and metabolic disorders such as hepatosteatosis.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
5CTCF is crucial to the organization of mammalian genomes into loop structures. According to recent studies, the transcription apparatus is compartmentalized and concentrated at super-enhancers to form phase-separated condensates and drive the expression of cell-identity genes. However, it remains unclear whether and how transcriptional condensates are coupled to higher-order chromatin organization. Here, we show that CTCF is essential for RNA polymerase II (Pol II)-mediated chromatin interaction
Our data indicate that liver-specific deletion of CTCF leads to hepatosteatosis through augmented PPARγ DNA-binding activity, which up-regulates its downstream target genes associated with the lipid metabolic process.
Dendritic cells are antigen-presenting cells orchestrating innate and adaptive immunity. The crucial role of transcription factors and histone modifications in the transcriptional regulation of dendritic cells has been extensively studied. However, it is not been well understood whether and how three-dimensional chromatin folding controls gene expression in dendritic cells. Here we demonstrate that activation of bone marrow-derived dendritic cells induces extensive reprogramming of chromatin loo
Natural killer (NK) cells are an essential part of the innate immune system that helps control infections and tumors. Recent studies have shown that Vorinostat, a histone deacetylase (HDAC) inhibitor, can cause significant changes in gene expression and signaling pathways in NK cells. Since gene expression in eukaryotic cells is closely linked to the complex three-dimensional (3D) chromatin architecture, an integrative analysis of the transcriptome, histone profiling, chromatin accessibility, an
CTCF (CCCTC-binding factor) is crucial for organizing mammalian genomes into domains and structural loops, yet its role in enhancer-promoter interactions remains unclear. Here, we demonstrate that 3D enhancer architecture undergoes marked reorganization upon CTCF depletion in activated CD4+ T cells. Despite this, active transcription, particularly driven by STAT5-bound super-enhancers, maintains enhancer loops independently of CTCF. Interestingly, robust enhancer-promoter interactions are associ