ZNF280C antibody
- Known as:
- ZNF280C (anti-)
- Catalog number:
- orb126511
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ZNF280C antibody
Related genes to: ZNF280C antibody
- 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 antibody
Related articles to: ZNF280C antibody
- Histone H4 lysine 20 trimethylation (H4K20me3) is a histone modification that is critical in maintaining genome integrity. Dysregulation of H4K20me3 and KMT5C, the major methyltransferase for H4K20me3, occurs commonly in multiple types of cancer but the mechanisms surrounding how they contribute to shaping the epigenomic landscape remains unclear. Here, we show that KMT5C is involved in non-canonical deposition of H4K20me3, independent of H3K9me3, which was previously recognized as a prerequisite for H4K20me3. This novel subtype of H4K20me3 lacks canonical repressive epigenetic signatures and instead overlaps with multiple activating marks. These activating modifications likely contribute to the dynamic changes in transcript levels upon loss of H4K20me3. The mechanism involved in recruiting KMT5C to these loci is independent of HP1, the factor reported to be involved in recruitment of KMT5C to heterochromatin marked with H3K9me3. Instead, biochemical analyses revealed ZNF280C to be a novel interacting partner of KMT5C, with ZNF280C localizing specifically at H3K9me3-/H4K20me3+ sites. Together, these results suggest a novel, non-canonical function of KMT5C-H4K20me3 that protects vulnerable regions of the genome from uncontrolled expression. - Source: PubMed
Publication date: 2026/05/14
Son JihyeShih Ching-HuaDavidson ChristinaUtturkar Sagar MMabe Nathaniel WGlaws AlexandraVertino Paula MKasinski Andrea L - 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