Ask about this productRelated genes to: CTCFL antibody
- Gene:
- CTCFL NIH gene
- Name:
- CCCTC-binding factor like
- Previous symbol:
- -
- Synonyms:
- dJ579F20.2, BORIS, CT27
- Chromosome:
- 20q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-08-25
Related products to: CTCFL antibody
Related articles to: CTCFL antibody
- Cryptorchidism is caused by a combination of environmental and genetic variables. This study aimed to identify cryptorchidism-associated susceptibility genes through bioinformatics approaches and validate their dynamic expression patterns in rat models, with the exploration of upstream transcriptional factor (TF) regulatory networks. - Source: PubMed
Publication date: 2026/03/17
Chen JianxunShen DanKong JianZhang YouboGe WenliangXian Hua - Cohesin- and CTCF-mediated chromatin loops facilitate enhancer-promoter and promoter-promoter interactions, but their impact on global gene regulation remains debated. Here we show that acute removal of cohesin or CTCF in mouse cells dysregulates hundreds of genes. Cohesin depletion primarily downregulates CBP/p300-dependent putative enhancer targets, whereas CTCF loss both up- and downregulates enhancer targets. Beyond loop anchoring, CTCF directly modulates transcription, acting as an activator or repressor depending on its binding position and orientation at promoters. Mechanistically, when activating, CTCF increases DNA accessibility and promotes RNA polymerase II recruitment; when repressing, it prevents RNA polymerase II binding without altering chromatin accessibility. Promoter-bound CTCF activates housekeeping genes essential for cell proliferation. CTCF's transcriptional activation function-but not its loop anchoring role-is shared with its vertebrate-specific paralog, CTCFL. These findings reconcile architectural and non-architectural roles of cohesin and CTCF, offering a unified model for their functions in enhancer-dependent and enhancer-independent transcription control. - Source: PubMed
Publication date: 2025/11/18
Narita TakeoKilic SinanHigashijima YoshikiScherer Natalie MPappas GeorgiosMaskey ElinaChoudhary Chunaram - Black patients with pancreatic ductal adenocarcinoma (PDAC) are less likely to have a major pathologic response (MPR) after neoadjuvant chemotherapy (NAC). Data suggest lower baseline carbohydrate antigen 19-9 (CA 19-9) among Black patients. Whether CA 19-9 nonproduction contributes to racial differences in NAC response was evaluated, and the biological mechanisms underlying the reduced response in CA 19-9 nonproducers (CAnonprod) were investigated. - Source: PubMed
Martos Mary PDickey Erin MAbdilleh KawtherAhmad Syed AMaithel Shishir KLeigh-Matijakovich NatashaKim Hong JinAbbott Daniel EZafar Syed NabeelKooby David AParikh Alexander AHosein Peter JMerchant Nipun BDatta JashodeepHester Caitlin A - Cancer-testis antigens (CTAs) are promising targets for immuno-oncotherapy. They offer the potential to treat cancers for which effective systemic therapies are lacking, including canine malignant melanoma (CMM). In this study, we investigate the suitability of eight canine orthologs of human CTAs as targets for immunotherapy, including cancer-associated gene 1 (CAGE1), CCCTC-binding factor (CTCFL), DEAD-box helicase 53 (DDX53), the melanoma antigen gene (MAGE), 5'-nucleotidase, cytosolic IB (NT5C1B), P antigen family member 3-like (PAGE3-like), preferentially expressed antigen in melanoma (PRAME), and synovial sarcoma X chromosome breakpoint (SSX). MAGE proteins were detected by immunohistochemistry in 12.1 % (4/33) of CMM cases, including digital and oral melanoma, with healthy tissue expression restricted to the testis. CTA mRNA was detected by Real-time PCR in canine testis and validated through gel electrophoresis and Sanger sequencing. MAGE, PAGE3-like, and PRAME mRNA were strongly expressed in canine oral melanoma and metastatic cell lines with restricted expression in normal tissues. CAGE1, CTCFL, DDX53, and SSX6 were only weakly expressed or absent in canine oral melanoma. CTCFL and DDX53 expression in healthy tissues was not restricted to the testis, as moderate expression was found in the kidney. These results suggest that dogs express CTAs, similar to humans, and thus CTAs may serve as a target for immunotherapy in dogs. - Source: PubMed
Publication date: 2025/05/06
Hindriks EstherBergmann WilhelminaRuiz Aitor MartínezDe Maria RaffaellaZandvliet Maurice M J MSijts Alice J A MBroere Femke - Lung adenocarcinoma (LUAD) is a highly heterogenous and aggressive form of non-small cell lung cancer (NSCLC). The use of genome-wide gene co-expression networks (GCNs) has been paramount to describe changes in the transcriptional regulatory programs found between diseased and healthy states of LUAD. Recently, studies have shown that multiple cancerous phenotypes share a distinct GCN architecture, suggesting that network topology holds promise for understanding disease pathology. However, conventional GCN inference methods struggle to capture the inherent context-specificity within a patient population, thus flattening its heterogeneity. To address this issue, the use of single-sample network (SSN) modelling has emerged as a promising solution into studying heterogeneous traits of cancer through network-based approaches. Here, we reconstructed patient-specific GCNs (n=334) using the LIONESS equation and mutual information as the network inference method. Unsupervised analysis revealed six novel LUAD subtypes based on inter-patient network similarity, each with distinct network motifs reflecting unique biological programs. Supervised analysis, employing regularized Cox regression, identified 12 genes (CHRDL2, SPP2, VAC14, IRF5, GUCY1B1, NCS1, RRM2B, EIF5A2, CCDC62, CTCFL, XG, and TP53INP2) whose weighted degree in SSNs is predictive of patient survival in LUAD. These findings suggest that topological features of SSNs offer valuable insights into the context-specific nature of LUAD malignancy, highlighting the potential of SSN-based approaches for further research. - Source: PubMed
Publication date: 2025/05/09
López-Sánchez PatricioÁvila-Moreno FedericoHernández-Lemus EnriqueKuijjer Marieke LEspinal-Enríquez Jesús