Ask about this productRelated genes to: CTCF antibody
- Gene:
- CTCF NIH gene
- Name:
- CCCTC-binding factor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-20
- Date modifiied:
- 2016-02-12
Related products to: CTCF antibody
Related articles to: CTCF antibody
- Topologically associating domains (TADs) are generally considered as a homogeneous basic units of genome folding, which is critical for transcriptional regulation. However, recent studies indicate that both the TAD domain structures and the boundaries between them are not as homogeneous as originally recognized. Here, we address the heterogeneity of the TAD boundaries in the human genome at a large scale, which varies between active and inactive chromatin and across cell lines and tissues. To address this, based on the well-annotated TAD boundaries extracted from multiple cell lines and tissues, we examine their nucleotide content, resulting in two main clusters, one GC-rich and one AT-rich, which are mainly distributed in active and inactive chromatin, respectively. Also, they contain different types of repetitive sequences and have different epigenetic patterns, with more CTCF binding motifs in the GC-rich cluster. Hence, our observations of the TAD boundary content provide novel insights into TAD genomic architecture. In addition, we find that cell- or tissue-specific boundaries are less evolutionarily conserved than other boundaries. We highlight the importance of TAD boundary diversity in different functional contexts and discuss the importance of the different types of repetitive sequences and epigenetic patterns in the two main types of boundaries. - Source: PubMed
Publication date: 2026/08/14
Sun YingTommerup NielsJensen Lars JuhlGorodkin Jan - Eukaryotic genomes self-organize into diverse three-dimensional (3D) chromatin conformations through intranuclear long-range interactions, yet it remains challenging to interpret how concurrent interactions combine along a chromatin polymer to shape measurable conformational readouts. Building on a minimal harmonic polymer model and the Gaussian covariance formalism, we present a 3D genome circuit representation that reorganizes the covariance-derived effective interaction strength (EIS) of a target locus pair into motif-level interaction patterns. In this representation, the graph topology of a chromatin interaction network determines the arrangement of circuit operations that summarize how local loop motifs contribute to EIS through series-like, parallel-like, or more general coupled-network combinations. The resulting EIS is then connected to experimentally accessible statistics, including pairwise contact probabilities and spatial-distance distributions from the Gaussian equilibrium ensemble, and loop stability through a first-passage description. Beyond single-pair readouts, we derive a closed-form Pearson correlation coefficient between two inter-locus spatial distances in a general harmonic network, providing an analytical way to quantify coordinated proximity changes between two locus pairs. We apply the framework to (i) estimate the effective Shh-ZRS interaction strength in a preformed CTCF-dependent loop configuration and (ii) quantify enhancer-promoter proximity coordination in a shared-enhancer configuration. This motif-level circuit representation provides physics-grounded design rules for interpreting how local interaction topology, interaction strength, and perturbations such as anchor deletion or tether addition alter EIS and associated 3D conformational readouts. - Source: PubMed
Publication date: 2026/08/14
Zhang ZhenquanWang ZihaoLuo SonghaoYu XiaochenTang ZhonghuiZhang Jiajun - Ischemic cardiomyopathy (ICM) is a condition characterized by inadequate blood supply to the coronary arteries, resulting in myocardial damage and decreased cardiac functionality. This study aimed to identify potential biomarkers and regulatory networks in ICM, providing a foundation for further mechanistic and therapeutic investigations. - Source: PubMed
Publication date: 2026/07/29
Ye XianhuaWu GuoxiangXie JialanWu YanqingChen DaqiuChen YixingXu ShanghuaLuo Shunxiang - The nuclear RNA exosome, a conserved 3'→5' ribonuclease complex, degrades the vast majority of RNA polymerase II output, including promoter upstream transcripts, enhancer RNAs, antisense transcripts, and retrotransposon-derived RNAs. Beyond this housekeeping role, the exosome acts as an epigenetic effector, and its dysfunction underlies a growing spectrum of human disease. Here we integrate recent structural, genomic, and disease-focused studies into a unified model of the exosome as a guardian of the epigenome. We describe how MTR4-containing adaptor complexes TRAMP, NEXT, and PAXT confer substrate selectivity, and how the exosome enforces heterochromatic silencing in concert with HP1 proteins and the Human Silencing Hub (HUSH) complex and preserves three-dimensional genome architecture at insulators and enhancers, such as the protocadherin locus where RNA surveillance, CTCF insulation, and heterochromatin converge. We then examine the consequences of failure: exosomopathies such as pontocerebellar hypoplasia, loss of DIS3- and PAXT-mediated tumor suppression in cancer, and age-related erosion of surveillance that permits transposable element de-repression, RIG-1/MDA5 and cGAS-STING-driven inflammation, cellular senescence, and neurodegeneration. We conclude that the exosome couples RNA decay to epigenetic state across the lifespan, positioning RNA surveillance as an emerging therapeutic target. - Source: PubMed
Publication date: 2026/07/30
Newman Andrew GSingh Prim B - Helicobacter pylori (H. pylori) infection triggers oxidative stress and persistent inflammatory responses, both of which lead to cellular DNA damage while impairing DNA repair. This constitutes a major factor in exacerbating inflammation and subsequently inducing precancerous lesions, with effective interventions still lacking. In our study, we found that bone marrow mesenchymal stem cell-conditioned medium (BMMSC-CM) could alleviate H. pylori-induced DNA damage in gastric mucosal epithelial cells and further corroborated in vivo studies through immunofluorescence staining and flow cytometry. Screening via solid-phase antibody arrays and transcriptome sequencing revealed that BMMSC up-regulated the expression of CTCF in gastric mucosal epithelial cells by secreting the glycoprotein CHI3L1, thereby enhancing Rad51 expression and promoting cellular DNA repair. Meanwhile, untargeted metabolomics and lipidomics further demonstrated that CTCF participated in the DNA repair process through CPT1A-mediated fatty acid oxidation. This study elucidated the role and application value of BMMSC-derived CHI3L1 in treating H. pylori-induced gastric mucosal damage. By exploring the specific mechanism through the regulation of fatty acid oxidation on DNA repair, this study provided new insights and potential therapeutic targets for treating H. pylori infection-related diseases. - Source: PubMed
Publication date: 2026/08/07
Qianqian WangXiaoxiao WangYongbin WangJing ChenZhang Hu