TCOF1 Antibody
- Known as:
- TCOF1 Antibody
- Catalog number:
- XW-8122
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TCOF1 Antibody
Related genes to: TCOF1 Antibody
- Gene:
- TCOF1 NIH gene
- Name:
- treacle ribosome biogenesis factor 1
- Previous symbol:
- -
- Synonyms:
- treacle, TCS
- Chromosome:
- 5q32-q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-21
- Date modifiied:
- 2018-02-13
Related products to: TCOF1 Antibody
Related articles to: TCOF1 Antibody
- This study aims to investigate the role of lactylation and m6A modification-related genes in the tumor microenvironment and immunotherapy for hepatocellular carcinoma (HCC) patients. RNA-sequence data and corresponding clinical information of HCC were obtained from the TCGA and ICGC datasets. LASSO Cox regression analysis was implied to construct a lactylation-m6A related prognostic model. The 7-gene signature was established and effectively stratified patients into high- and low-risk groups. Further analysis revealed significant differences between the two risk groups in terms of tumor microenvironment, expression levels of immune checkpoint genes, and drug responsiveness. Specifically, the high-risk group exhibited increased immune cell infiltration, lower IC50 values for several drugs including 5-fluorouracil, afatinib, crizotinib, cediranib, taselisib, and staurosporine; Whereas the low-risk group displayed reduced stromal component proportions and better responses to entinostat, irinotecan, KRAS inhibitors, cisplatin, axitinib, and topotecan. Functionally, knockdown of TCOF1 and HDAC1 significantly attenuated the migration and invasive capacity of Huh-7cells. The lactylation-m6A related prognostic model exhibited robust predictive efficiency in HCC. TCOF1 and HDAC1 may be promising tumor biomarkers for HCC and more researches are needed to validate these results. - Source: PubMed
Publication date: 2026/05/02
Zhang ShaohuiLiu JianhuaGuan JunRen Huili - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. The lack of reliable biomarkers to predict treatment response limits patient stratification and personalized therapy. Extracellular vesicles (EVs) represent a minimally invasive source of tumor-derived proteins that may reflect treatment-relevant biological changes. This study investigated EV-based protein profiling in HCC patients undergoing high-dose conformal radiotherapy to identify prognostic biomarkers associated with treatment response and overall survival. - Source: PubMed
Publication date: 2026/04/04
Puhr-Westerheide DanielÖcal ElifHirner-Eppeneder HeidrunCorradini StefanieSalvermoser LukasStechele MatthiasBen Khaled NajibPiseddu IgnazioWildgruber MoritzSeidensticker MaxRicke JensFabritius Matthias PhilippAlunni-Fabbroni Marianna - To elucidate the prenatal diagnostic challenges, genetic landscape, and clinical outcomes of Treacher Collins syndrome (TCS), focusing on the role of variants, prenatal ultrasound findings, and counselling implications. - Source: PubMed
Publication date: 2026/03/19
Li ChunlingHuang WeiGan ZhongzhiLing YinQiu LiyanXiao YuanlingXiong FuYang Fang - TCOF1 is a nucleolar protein involved in ribosome biogenesis, DNA damage response, and mitotic regulation. Germline mutations are associated with Treacher-Collins syndrome, a rare congenital disorder characterized by craniofacial abnormalities. Clear cell renal cell carcinoma (ccRCC), the most prevalent form of kidney cancer, exhibits pronounced nuclear and nucleolar pleomorphism, which correlates with tumour aggressiveness. The ccRCC grading system relies on microscopic evaluation of nuclear and nucleolar features. Here, we hypothesized that TCOF1 contributes to ccRCC tumorigenesis. - Source: PubMed
Publication date: 2026/03/17
Grzanka MałgorzataPopławski PiotrWiśniewski Jacek RIwanicka-Nowicka RoksanaKossowska HelenaKoblowska MartaRybicka BeataBiałas AlexPiekiełko-Witkowska Agnieszka - : Ankylosis of the temporomandibular joint (TMJ) is a rare developmental disorder that involves fibrous or bony fusion within the joint. It is a severe structural and functional disorder. Typically, the phenotype manifests as joint immobilization and results in facial deformity and trismus. To date, ankylosis is rarely diagnosed as congenital and its occurrence mechanism has not been thoroughly understood. We observed a female patient who as a newborn showed slight facial asymmetry and impaired mandibular retraction. In addition, non-uniform occlusal fissures were noted; the lower part of the left earlobe was slightly smaller than the right earlobe. The aim of the work was the identification of pathogenic variants in the genome related to ankylosis. Ankylosis has no known causative gene yet; thus, Whole Exome Sequencing (WES) was performed. : We observed a female patient with facial asymmetry and impaired mandibular retraction from birth. No phenotypic abnormalities were noted on the head or elsewhere on the body. A diagnostic computed tomography (CT) scan of the head performed at five months of age led to the diagnosis of congenital zygomatic-coronoid ankylosis. Genomic DNA samples were subjected to WES. Library preparation was carried out using the Twist Library Preparation EF Kit 2.0, followed by target enrichment with the Twist Exome 2.0 Plus Comprehensive Exome. Sequencing reads were aligned to the human reference genome (GRCh38), and variant calling was performed using standard bioinformatics workflows. Variants were subsequently filtered, annotated, and interpreted using VariantStudio. Assessment of variant pathogenicity was primarily based on comparisons with public databases, including ClinVar and VarSome, and was supported by in silico prediction tools such as SIFT and PolyPhen-2. : In genes responsible for disorders of the I and II pharyngeal arches, three pathogenic variants were identified: in the genes TCOF1 and POLR1B, responsible for the development of Treacher Collins syndrome (TCS), and one in the DHODH gene, responsible for Miller syndrome. Additionally, in genes that have not been linked so far with rare facial disorders, 42 variants were identified, of which 8 are listed as pathogenic. We present the first described patient with congenital ankylosis, who, although showing no phenotypic features of these syndromes, has identified pathogenic variants in genes responsible for craniofacial dysostosis. : Variants in TCOF1, POLR1B and DHODH may represent candidate genetic factors associated with susceptibility to ankylosis. WES analysis is an appropriate method in the case of patients with congenital diseases with unknown genetic origin. In this study we provide a comprehensive list of all identified pathogenic variants. This might be useful for scientists searching for the genetic background of skeletal system issues, one of which could be bone and fibrous tissue remodeling. - Source: PubMed
Publication date: 2026/02/11
Marszałek-Kruk Bożena AnnaDowgierd KrzysztofLejawa MateuszKulesa-Mrowiecka MałgorzataWolański WojciechMyśliwiec AndrzejLipowicz Anna