CTCF EMSA Probe Set
- Known as:
- CTCF EMSA Probe Set
- Catalog number:
- AY1179P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- CTCF EMSA Probe Set
Related genes to: CTCF EMSA Probe Set
- 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 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: CTCF EMSA Probe Set
- Cohesin-NIPBL complexes extrude genomic DNA into loops that are constrained by CTCF boundaries. This process has important regulatory functions and weakens the separation between euchromatic and heterochromatic compartments. Cohesin can also bind PDS5 proteins, which do not support loop extrusion but are required for the formation of CTCF boundaries. How PDS5 proteins perform this function is unknown. Here we show, by in vitro single-molecule imaging, that human PDS5 proteins stop loop extrusion by facilitating the dissociation of NIPBL from cohesin. Hi-C experiments suggest that this function is required for the establishment of CTCF boundaries in cells. In silico modeling indicates that PDS5 proteins enable the separation between compartments by limiting cohesin's velocity and chromatin residence time. The degree of this compartmentalization depends on the frequency with which chromatin is extruded relative to the time it takes for compartments to form. These results identify PDS5 proteins as key regulators of genome organization. - Source: PubMed
Publication date: 2026/04/23
Wutz GordanaDavidson Iain FBanigan Edward JStocsits Roman RKawasumi RyotaroTang WenNagasaka KotaCostantino LorenzoJansen RalfHirota KoujiBranzei DanaMirny Leonid APeters Jan-Michael - Accumulating evidence indicates that mitochondrial dysfunction is a hallmark of cancer. Nonetheless, the mechanisms linking mitochondrial dysfunction to cancer progression remain largely elusive. SLC25A48 was recently recognized as a transporter involved in mitochondrial choline uptake. Nevertheless, the roles of SLC25A48 in human malignancies remain unexplored. Here, we found that SLC25A48 is elevated in colorectal cancer (CRC) tissues and associates with unfavorable patient outcomes. Functional analyses showed that SLC25A48 accelerates the growth of CRC by enhancing proliferative capacity and preventing cell death. Mechanistically, SLC25A48 exerts its oncogenic function by enhancing the synthesis of choline-derived betaine, which is an important source of one-carbon units for numerous biosynthetic processes. On the one hand, SLC25A48 mitigates oxidative stress-induced ferroptosis by augmenting NADPH availability. On the other hand, it enhances cell proliferation by promoting mitochondrial energy production through upregulating mitochondrial DNA (mtDNA) replication and transcription. Importantly, silencing of SLC25A48 augmented the responsiveness of CRC cells to RSL3-induced ferroptosis and 5-FU-based chemotherapy. Furthermore, increased CTCF expression may contribute, at least in part, to the upregulation of SLC25A48 in CRC. Collectively, our data emphasize that SLC25A48 plays a critical oncogenic role in CRC and holds potential as a druggable target to overcome drug resistance in CRC. - Source: PubMed
Publication date: 2026/04/20
Wang ZhenHe JinghuJifu EYang YingYang Xiaohong - The human spinal cord controls sophisticated sensory perception and motor response across its extensive length. However, the spatial and temporal regulation of the generation of various motor neurons (MNs) and glial cells remains obscure. Using single-cell RNA sequencing (scRNA-seq) and single-cell Stereo RNA sequencing (scStereo RNA-seq), we here investigated and annotated molecular signatures of three neural stem cell (NSC) lineages, MNs, astrocytes, and oligodendrocytes, in the human fetal spinal cord from gestational week 8 (GW8) to GW12. We also found that some long noncoding RNAs (lncRNAs) have overlapping or reciprocal expression patterns with their adjacent coding genes, which are enriched with the promoter, enhancer, and CCCTC-binding factor (CTCF) in the same cell cluster. Our study generated a rich spatial expression library of molecular diversity of lncRNAs and their adjacent genes in neurons and glia in the human fetal spinal cord. - Source: PubMed
Publication date: 2026/03/17
Miao NanLee TrevorChen LiyingZhang HeganWang JingSun JulianneSun JasonSha YongqiangHuang Shi-YingSun Tao - Tumor cell fraction (TCF) estimation is an essential step in homologous recombination deficiency (HRD) testing of tubo-ovarian high-grade serous carcinoma (HGSC). However, it is prone to variability and observer dependence. Here, we assess the reliability of the QuANTUM computational pipeline for TCF estimation (cTCF) in HGSC samples. 70 HGSC cases were retrospectively collected and the AmoyDx HRD Focus Panel was employed for DNA extraction and sequencing. TCF estimates were obtained from multiple pathologists, along with the TCF calculated by the proprietary AmoyDx algorithm. The QuANTUM pipeline-derived cTCF and a manually calculated ground truth (GT) were obtained on the same slides, and concordance analyses were performed. Weighted kappa (Wk) values for the agreement among the various pathologists ranged from 0.28 to 0.63, reflecting low to substantial concordance. The QuANTUM algorithm showed substantial and better agreement with the GT and the AmoyDx tool (Wk = 0.73 and 0.63, respectively) as compared to the pathologists' estimates. No significant differences were observed between QuANTUM, the GT and the AmoyDx tool in identifying cases with tumor cellularity above or below the method-defined 30% cutoff. Considering its high reliability, the QuANTUM algorithm may serve as a robust tool for ensuring adequate TCF evaluation in HGSC. - Source: PubMed
Publication date: 2026/04/18
Alviano Antonio MariaPagni FabioSeminati DavideCasati GabrieleJaconi MartaFruscio RobertDe Leo AntonioMaloberti ThaisL'Imperio VincenzoDe Biase DarioCazzaniga Giorgio - The three-dimensional organization of eukaryotic genomes into compartments, topologically associating domains, and loops is mediated by architectural proteins whose organizational principles vary across species. In , insulator proteins including Su(Hw) and the histone variant γH2Av form liquid-liquid phase separation (LLPS) condensates, yet how this phase separation capacity relates to genome compartmentalization has remained unclear. Here we use hyperosmotic stress to simultaneously displace architectural proteins from chromatin in both and human cells, enabling a comparative dissection of genome organization principles across species. We find that although human CTCF shares predicted LLPS properties with insulator proteins, it does not form condensates upon osmotic stress, while insulator proteins do. Hi-C analysis reveals that osmotic stress causes loss of compartments, TAD boundary strength, and loops in both organisms, but genome recovery after stress is rapid and near-complete in human cells while remaining substantially incomplete in after one hour. Analysis of this recovery asymmetry reveals a fundamental difference in compartment organization: whereas human A and B compartments engage in robust homotypic long-range interactions, B compartments rarely participate in long-range B-to-B contacts, indicating that the genome does not replicate canonical A/B compartment organization. Instead, genome architecture is dominated by A-to-A interactions, and A compartments are specifically enriched in γH2Av and Su(Hw), with moderate enrichment of cohesin subunits. Furthermore, loops in are mechanistically independent from compartments and TADs, recovering before compartment structure is restored, and are anchored by Su(Hw) and cohesin rather than by dCTCF. Together, these findings suggest that the LLPS properties of γH2Av and Su(Hw) underlie A compartment formation in through a mechanism distinct from the heterochromatin-driven B compartment interactions that predominate in vertebrates, revealing fundamentally different organizational principles between fly and human genomes. - Source: PubMed
Publication date: 2026/04/06
Amankwaa BrightPlayter ChristopherStow EmilySanders Jacob TXue TianchunMcCord Rachel PattonLabrador Mariano