ZNF545 antibody - C-terminal region (ARP31893_P050)
- Known as:
- ZNF545 (anti-) - C-terminal region (ARP31893_P050)
- Catalog number:
- arp31893_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF545 antibody - C-terminal region (ARP31893_P050)
Related genes to: ZNF545 antibody - C-terminal region (ARP31893_P050)
- Gene:
- ZFP82 NIH gene
- Name:
- ZFP82 zinc finger protein
- Previous symbol:
- ZNF545
- Synonyms:
- MGC45380, KIAA1948
- Chromosome:
- 19q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-13
- Date modifiied:
- 2014-11-19
Related products to: ZNF545 antibody - C-terminal region (ARP31893_P050)
Related articles to: ZNF545 antibody - C-terminal region (ARP31893_P050)
- Current methods for cholangiocarcinoma (CCA) detection in primary sclerosing cholangitis (PSC) lack accuracy, often leading to late, non-curative diagnoses. This study aimed to identify DNA methylation biomarkers in liquid biopsies for earlier and more accurate CCA detection. - Source: PubMed
Publication date: 2026/04/29
Vedeld Hege MarieBreder SigurdPharo HeidiBrodal Hans PetterAdolfsen Evy MarieBrandt-Winge Saravon Seth ErikGrimsrud Marit MæhleYaqub SherazKarlsen Tom HGrzyb KrzyztofPaulsen VemundFärkkilä Martti ABergquist AnnikaAabakken LarsBoberg Kirsten MFolseraas TrineLind Guro E - Tumor suppressor genes silenced by CpG methylation uncover the molecular mechanism of tumorigenesis and potential tumor biomarkers. Our previous research found that the promoter of zinc-finger protein 82 (ZFP82) was highly methylated in multiple cancers, including esophageal cancer, which induces the occurrence and development of tumors. Here, we describe the frequent detection of methylation of the ZFP82 promoter CpG Island in patients who did not respond to neoadjuvant chemotherapy, indicating that ZFP82 may related to esophageal cancer chemo-resistance. We further verified that in esophageal cancer cells expressing wild-type p53, ZFP82 bound to the HDAC3 promoter and mediated its interaction with p53, leading to HDAC3 cleavage and reduction of p53 ubiquitin-dependent proteasomal degradation, thus enhancing wild-type p53 stability. In cells expressing mutant p53, ZFP82 interacted with HDAC3 to regulate the down-regulation of HSP 70, leading to degradation of mutant p53. Through both mechanisms, the restoration of ZFP82 enhanced the chemosensitivity in esophageal cancer cells expressing wild-type p53 or mutant p53, significantly inhibiting in vivo tumorigenicity of these cells. Analyses of the expression of ZFP82 and clinical data indicated that ZFP82 expression correlated with improved prognosis. Our results define a mechanism for p53 stabilization via ZFP82-dependent HDAC3 decay under genotoxic stress conditions and validate a candidate bio-marker of early prediction of patients who will respond to esophageal cancer neoadjuvant chemotherapy. - Source: PubMed
Publication date: 2025/10/06
Peng WeiyanWang HongpengSun XuejuanXu ZhongZhang LingxiangYe Lin - Identifying genetic determinants of reproductive success may highlight mechanisms underlying fertility and identify alleles under present-day selection. Using data in 785,604 individuals of European ancestry, we identified 43 genomic loci associated with either number of children ever born (NEB) or childlessness. These loci span diverse aspects of reproductive biology, including puberty timing, age at first birth, sex hormone regulation, endometriosis and age at menopause. Missense variants in ARHGAP27 were associated with higher NEB but shorter reproductive lifespan, suggesting a trade-off at this locus between reproductive ageing and intensity. Other genes implicated by coding variants include PIK3IP1, ZFP82 and LRP4, and our results suggest a new role for the melanocortin 1 receptor (MC1R) in reproductive biology. As NEB is one component of evolutionary fitness, our identified associations indicate loci under present-day natural selection. Integration with data from historical selection scans highlighted an allele in the FADS1/2 gene locus that has been under selection for thousands of years and remains so today. Collectively, our findings demonstrate that a broad range of biological mechanisms contribute to reproductive success. - Source: PubMed
Publication date: 2023/03/02
Mathieson IainDay Felix RBarban NicolaTropf Felix CBrazel David M Vaez Ahmadvan Zuydam NatalieBitarello Bárbara DGardner Eugene JAkimova Evelina TAzad AjunaBergmann SvenBielak Lawrence FBoomsma Dorret IBosak KristinaBrumat MarcoBuring Julie ECesarini DavidChasman Daniel IChavarro Jorge ECocca MassimilianoConcas Maria PinaDavey Smith GeorgeDavies GailDeary Ian JEsko TõnuFaul Jessica D Franco OscarGanna AndreaGaskins Audrey JGelemanovic Andreade Geus Eco J CGieger ChristianGirotto GiorgiaGopinath BaminiGrabe Hans JörgenGunderson Erica PHayward CarolineHe Chunyanvan Heemst DianaHill W DavidHoffmann Eva RHomuth GeorgHottenga Jouke JanHuang HongyangHyppӧnen ElinaIkram M ArfanJansen RickJohannesson MagnusKamali ZohaKardia Sharon L RKavousi MaryamKifley AnnetteKiiskinen TuomoKraft PeterKühnel BrigitteLangenberg ClaudiaLiew Gerald Lind Penelope ALuan Jian'anMägi ReedikMagnusson Patrik K EMahajan AnubhaMartin Nicholas GMbarek HamdiMcCarthy Mark IMcMahon GeorgeMedland Sarah EMeitinger ThomasMetspalu AndresMihailov EvelinMilani LiliMissmer Stacey AMitchell PaulMøllegaard StineMook-Kanamori Dennis OMorgan Annavan der Most Peter Jde Mutsert RenéeNauck MatthiasNolte Ilja MNoordam RaymondPenninx Brenda W J HPeters AnnettePeyser Patricia APolašek OzrenPower ChrisPribisalic AjkaRedmond PaulRich-Edwards Janet WRidker Paul MRietveld Cornelius ARing Susan MRose Lynda MRueedi RicoShukla VallariSmith Jennifer AStankovic StasaStefánsson KáriStöckl DorisStrauch KonstantinSwertz Morris ATeumer AlexanderThorleifsson GudmarThorsteinsdottir UnnurThurik A RoyTimpson Nicholas JTurman ConstanceUitterlinden André GWaldenberger MelanieWareham Nicholas JWeir David RWillemsen GonnekeZhao Jing HauZhao WeiZhao YajieSnieder Haroldden Hoed MarcelOng Ken KMills Melinda CPerry John R B - Ribosome biogenesis plays a pivotal role in tumorigenesis by supporting robust protein translation. We investigate the functional and molecular mechanism of Zinc finger protein 545 (ZNF545), a transcriptional repressor for ribosomal RNA (rRNA), in colorectal cancer (CRC). ZNF545 was silenced in CRC compared to adjacent normal tissues (P < 0.0001), implying a tumor-suppressive role. Colon-specific Znf545 knockout in mice accelerated CRC in Apc and azoxymethane/dextran sulfate sodium-induced CRC. Mechanistically, we demonstrated that ZNF545 uses its two zinc finger clusters to bind to minimal rDNA promoter, where it assembled transcriptional repressor complex by interacting with KAP1. Znf545 deletion in mouse embryonic fibroblasts not only increased rRNA transcription rate and the nucleolar size and number but also altered the nucleolar composition and architecture with an increased number of fibrillar centers surrounded by net-like dense fibrillar components. Consequently, Znf545 deletion promoted the gene expression of translation machinery, protein translation, and cell growth. Consistent with its tumor-suppressive role, ZNF545 overexpression in CRC cells induced growth arrest and apoptosis. Finally, administration of rRNA synthesis inhibitor, CX-5461, inhibited CRC development in Znf545Apc mice. In conclusion, ZNF545 suppresses CRC through repressing rRNA transcription and protein translation. Targeting rRNA biosynthesis in ZNF545-silenced tumors is a potential therapeutic strategy for CRC. - Source: PubMed
Publication date: 2021/10/06
Wang ShiyanWong Chi ChunZhang YanquanHuang JunzheLi ChuangenZhai JianningWang GuopingWei HongZhang XuejiHe Housheng HansenYu Jun - Pancreatic cancer remains one of the chief contributors to cancer related deaths on a global scale, with its diagnosis often associated with poor prognosis and high mortality. Accumulating literature continues to highlight the role of aberrant DNA methylation in relation to pancreatic cancer progression. Integrated bioinformatics approaches in the characterization of methylated-differentially expressed genes (MeDEGs) in pancreatic cancer were employed to enhance our understanding of the potential underlying molecular mechanisms of this cancer. We initially identified differentially expressed genes (DEGs) between 178 pancreatic cancer samples and 4 normal samples and differentially methylated genes (DMGs) based on 185 pancreatic cancer samples as well as 10 normal samples by analyzing RNA sequencing data in the TCGA database. Eventually, 31 MeDEGs including 5 hypomethylated/upregulated genes and 26 hypermethylated/downregulated genes were identified. Univariate Cox model and Kaplan-Meier method revealed that, among 31 MeDEGs, 5 hypermethylated/downregulated genes (ZNF804A, ZFP82, TRIM58, SOX17, and C12orf42) were correlated with poor survival of patients with pancreatic cancer. KEGG pathway enrichment analysis by GSEA 3.0 and the protein-protein interaction (PPI) network revealed that these 5 MeDEGs were enriched in numerous cancer-related pathways in addition to interacting with each other, highlighting a significant role in the development of pancreatic cancer. Taken together, the key findings of the current study demonstrate that ZNF804A, ZFP82, TRIM58, SOX17, and C12orf42 are hypermethylated/downregulated genes in pancreatic cancer and may be associated, through their modulation of specific pathways, with unfavorable pancreatic cancer prognosis. - Source: PubMed
Publication date: 2021/03/23
Sun HaifengXin RuiZheng ChangjunHuang Ge