Ask about this productRelated genes to: ZNF280C Blocking Peptide
- Gene:
- ZNF280C NIH gene
- Name:
- zinc finger protein 280C
- Previous symbol:
- SUHW3
- Synonyms:
- FLJ20095, ZNF633, ZPET
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-02
- Date modifiied:
- 2019-03-21
Related products to: ZNF280C Blocking Peptide
Related articles to: ZNF280C Blocking Peptide
- Hemophilia A (HA) is an X-linked recessive inherited bleeding disorder that typically affects men. Women are usually asymptomatic carriers, and rarely presenting with severe or moderately severe phenotype. This study aims to describe a case of a 17-year-old girl with moderate HA, investigating the mechanisms of her condition and the genetic basis within her family. - Source: PubMed
Publication date: 2025/01/06
Tan XiaoyanYang YiWu XiaZhu JingWang TengJiang HuihuiChen ShuLou Shifeng - The mRNA markers identified using microarray assay and diffusion tensor magnetic resonance imaging (DTI) were applied to elucidate the pathophysiology of attention-deficit hyperactivity disorder (ADHD). First, we obtained total RNA from leukocytes from three children with ADHD and three healthy controls for analysis with microarray assays. Subsequently, we applied real-time quantitative polymerase chain reaction (qRT‒PCR) assays to validate the differential expression of 7 genes (COX7B, CYCS, TFAM, UTP14A, ZNF280C, IFT57 and NDUFB5) between 130 ADHD patients and 70 controls, and we built an ADHD prediction model based on the ΔCt values of aforementioned seven genes (AUROC = 0.98). Finally, in a validation group (28 patients with ADHD and 27 healthy controls), mRNA expression of the above seven genes also significantly differentiated ADHD patients from controls (AUROC value = 0.91). The DTI analysis showed increased fractional anisotropy (FA) of the forceps minor, superior corona radiata, posterior corona radiata and anterior corona radiata in ADHD patients. Moreover, the FA of the right superior corona radiata tract was positively correlated with ΔCt levels of the COX7B gene and the IFT57 gene. The results shed a new light on a genetic profile of ADHD that may help in deciphering the white matter microstructural features in disease pathogenesis. - Source: PubMed
Publication date: 2024/02/21
Wang Liang-JenLi Sung-ChouChou Wen-JiunKuo Ho-ChangLee Sheng-YuLin Wei-Che - Dysregulated epigenetic and transcriptional programming due to abnormalities of transcription factors (TFs) contributes to and sustains the oncogenicity of cancer cells. Here, we unveiled the role of zinc finger protein 280C (ZNF280C), a known DNA damage response protein, as a tumorigenic TF in colorectal cancer (CRC), required for colitis-associated carcinogenesis and Apc deficiency–driven intestinal tumorigenesis in mice. Consistently, ZNF280C silencing in human CRC cells inhibited proliferation, clonogenicity, migration, xenograft growth, and liver metastasis. As a C2H2 (Cys2-His2) zinc finger-containing TF, ZNF280C occupied genomic intervals with both transcriptionally active and repressive states and coincided with CCCTC-binding factor (CTCF) and cohesin binding. Notably, ZNF280C was crucial for the repression program of trimethylation of histone H3 at lysine 27 (H3K27me3)-marked genes and the maintenance of both focal and broad H3K27me3 levels. Mechanistically, ZNF280C counteracted CTCF/cohesin activities and condensed the chromatin environment at the cis elements of certain tumor suppressor genes marked by H3K27me3, at least partially through recruiting the epigenetic repressor structural maintenance of chromosomes flexible hinge domain-containing 1 (SMCHD1). In clinical relevance, ZNF280C was highly expressed in primary CRCs and distant metastases, and a higher ZNF280C level independently predicted worse prognosis of CRC patients. Thus, our study uncovered a contributor with good prognostic value to CRC pathogenesis and also elucidated the essence of DNA-binding TFs in orchestrating the epigenetic programming of gene regulation. - Source: PubMed
Publication date: 2022/05/23
Ying YingWang MaolinChen YonghengLi MeiqiMa CanjieZhang JunbaoHuang XiaoyanJia MinZeng JunhuiWang YejunLi LiliWang XiaomeiTao QianShu Xing-Sheng - Skeletal muscle is highly plastic and dynamically regulated by the body's physical demands. This study aimed to determine the plasticity of skeletal muscle DNA methylation in response to 8 weeks of supervised exercise training in volunteers with a range of insulin sensitivities. We studied 13 sedentary participants and performed euglycemic hyperinsulinemic clamps with basal vastus lateralis muscle biopsies and peak aerobic activity (VO2 peak) tests before and after training. We extracted DNA from the muscle biopsies and performed global methylation using Illumina's Methylation EPIC 850K BeadChip. Training significantly increased peak aerobic capacity and insulin-stimulated glucose disposal. Fasting serum insulin and insulin levels during the steady state of the clamp were significantly lower post-training. Insulin clearance rates during the clamp increased following the training. We identified 13 increased and 90 decreased differentially methylated cytosines (DMCs) in response to 8 weeks of training. Of the 13 increased DMCs, 2 were within the following genes, , and . Of the 90 decreased DMCs, 9 were within the genes , , , , , , , , and . Moreover, pathway analysis showed an enrichment in metabolic and actin-cytoskeleton pathways for the decreased DMCs, and for the increased DMCs, an enrichment in signal-dependent regulation of myogenesis, NOTCH2 activation and transmission, and SMAD2/3: SMAD4 transcriptional activity pathways. Our findings showed that 8 weeks of exercise training alters skeletal muscle DNA methylation of specific genes and pathways in people with varying degrees of insulin sensitivity. - Source: PubMed
Publication date: 2022/03/02
Garcia Luis AZapata-Bustos RocioDay Samantha ECampos BaltazarHamzaoui YassinWu LindaLeon Alma DKrentzel JudithColetta Richard LDe Filippis EleannaRoust Lori RMandarino Lawrence JColetta Dawn K - Numerous DNA repair and signaling proteins function at DNA damage sites to protect the genome. Here, we show that fusion of the promiscuous biotin ligase BirA with RAD18 leads to localized protein biotinylation at DNA damage sites, allowing identification of ZPET (zinc finger protein proximal to RAD eighteen)/ZNF280C as a potential DNA damage response (DDR) protein. ZPET binds ssDNA and localizes to DNA double-strand breaks (DSBs) and stalled replication forks. In vitro, ZPET inhibits MRE11 binding to ssDNA. In cells, ZPET delays MRE11 binding to chromatin after DSB formation and slows DNA end resection through binding ssDNA. ZPET hinders resection independently of 53BP1 and HELB. Cells lacking ZPET displayed enhanced homologous recombination (HR), accelerated replication forks under stress, and increased resistance to DSBs and PARP inhibition. These results not only reveal ZPET as an HR repressor but also suggest that localized protein biotinylation at DNA damage sites is a useful strategy to identify DDR proteins. - Source: PubMed
Publication date: 2018/12/19
Moquin David MGenois Marie-MichelleZhang Jia-MinOuyang JianYadav TribhuwanBuisson RémiYazinski Stephanie ATan JunBoukhali MyriamGagné Jean-PhilippePoirier Guy GLan LiHaas WilhelmZou Lee