Ask about this productRelated genes to: ZNF205 Blocking Peptide
- Gene:
- ZNF205 NIH gene
- Name:
- zinc finger protein 205
- Previous symbol:
- ZNF210
- Synonyms:
- Zfp13
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2014-11-19
Related products to: ZNF205 Blocking Peptide
Related articles to: ZNF205 Blocking Peptide
- The tumor suppressor p53 is frequently dysregulated in cancer, whereas the mechanisms underlying its functional impairment remain unclear. Our previously identified KRAB domain-containing zinc finger proteins (KZFPs) as key p53 regulators in tumorigenesis and progression, specific members and their cancer-relevant mechanistic roles require further characterization. Here, we identified ZNF205, an SQ/TQ motif-bearing KZFP, as a critical oncogenic regulator in HCC. The pan-cancer analysis related to revealed that ZNF205 is an unfavorable prognostic factor for p53 wild-type patients with hepatocellular carcinoma (HCC). ZNF205 interacts with p53 and significantly inhibits its transcriptional activity by impeding the binding of p53 to target genes. Overexpression and knockdown of ZNF205 increase and decrease the malignant phenotype of HCC cells in a p53-dependent manner both in vitro and in vivo, respectively. Our study unveils ZNF205 as a novel p53 regulator and establishes its pro-tumorigenic function in HCC. These results reveal a novel p53 dysregulation mechanism in HCC and expand known KZFP-mediated p53 inactivation pathways, nominating ZNF205 as a therapeutic target to restore p53 function in HCC. - Source: PubMed
Publication date: 2026/02/10
Huang XiaofenYang YingchuanMa YuanHao WeiJin JingzhuoDing YueZhang YimingZhang XiuyuanLi XinliSong QinLiu JiaqiLiu BingxinZhai YuanjunZhao ChunlingWu JinTian Chunyan - Long non-coding RNAs (lncRNAs) are frequently reported to involve in the onset and development of non-small cell lung cancer (NSCLC). Cisplatin (DDP) resistance continues to pose a daunting challenge for improving the prognosis of NSCLC patients. The current study intends to elucidate the molecular mechanisms underlying the function of lncRNA ZNF205 AS1/early growth response 4 (EGR4) positive feedback loop in DDP resistance of NSCLC. - Source: PubMed
Publication date: 2024/01/15
Li HaiyanJin YingyingZhu YefeiShen BingxiaoXu Youzu - Retinoic acid-inducible gene I (RIG-I) is a cytosolic viral RNA receptor. Upon viral infection, the protein recognizes and then recruits adapter protein mitochondrial antiviral signaling (MAVS) protein, initiating the production of interferons and proinflammatory cytokines to establish an antiviral state. In the present study, we identify zinc finger protein 205 (ZNF205) which associates with RIG-I and promotes the Sendai virus (SeV)-induced antiviral innate immune response. Overexpression of ZNF205 facilitates interferon-beta (IFN-β) introduction, whereas ZNF205 deficiency restricts its introduction. Mechanistically, the C-terminal zinc finger domain of ZNF205 interacts with the N-terminal tandem caspase recruitment domains (CARDs) of RIG-I; this interaction markedly promotes K63 ubiquitin-linked polyubiquitination of RIG-I, which is crucial for RIG-I activation. Thus, our results demonstrate that ZNF205 is a positive regulator of the RIG-I-mediated innate antiviral immune signaling pathway. - Source: PubMed
Zhong NiWang ChenWeng GuangxiuLing TingXu Liangguo - Accumulating evidences revealed that long noncoding RNAs (lncRNAs) are frequently implicated in non-small cell lung cancer (NSCLC). Herein, we reported the identification of a novel NSCLC-associated functional lncRNA ZNF205 antisense RNA 1 (ZNF205-AS1). ZNF205-AS1 was increased in NSCLC tissues and cell lines, and associated with poor prognosis of NSCLC patients. Bioinformatics prediction, combined with experimental verification revealed that early growth response 4 (EGR4) directly bound to ZNF205-AS1 promoter, increased the promoter activity of ZNF205-AS1, and activated ZNF205-AS1 transcription. Intriguingly, ZNF205-AS1 transcript directly interacted with EGR4 mRNA, increased EGR4 mRNA stability, and up-regulated EGR4 expression via RNA-RNA interaction. Thus, ZNF205-AS1 and EGR4 formed a positive feedback loop. Through regulating EGR4, ZNF205-AS1 activated its own promoter activity. EGR4 was also increased in NSCLC and the expression of ZNF205-AS1 was significantly positively correlated with EGR4 in NSCLC tissues. Gain-of-function and loss-of-function assays demonstrated that both ZNF205-AS1 and EGR4 promoted NSCLC cell growth in vitro and NSCLC tumour growth in vivo. Concurrently depleting ZNF205-AS1 and EGR4 more significantly repressed NSCLC tumour growth in vivo. Collectively, our study demonstrated that the positive feedback loop between ZNF205-AS1 and EGR4 promotes NSCLC growth, and implied that targeting this feedback loop may be promising therapeutic strategy for NSCLC. - Source: PubMed
Publication date: 2018/12/16
He SusuLin JianXu YouzuLin LingFeng Jiaxi - Using genome-wide small interfering RNA (siRNA) screens for poliovirus, influenza A virus and rotavirus, we validated the top 6 gene hits PV, RV or IAV to search for host genes that when knocked-down (KD) enhanced virus permissiveness and replication over wild type Vero cells or HEp-2 cells. The enhanced virus replication was tested for 12 viruses and ranged from 2-fold to >1000-fold. There were variations in virus-specific replication (strain differences) across the cell lines examined. Some host genes (CNTD2, COQ9, GCGR, NDUFA9, NEU2, PYCR1, SEC16G, SVOPL, ZFYVE9, and ZNF205) showed that KD resulted in enhanced virus replication. These findings advance platform-enabling vaccine technology, the creation of diagnostic cells substrates, and are informative about the host mechanisms that affect virus replication in mammalian cells. - Source: PubMed
Publication date: 2017/11/27
Murray JackelynTodd Kyle VBakre AbhijeetOrr-Burks NicholeJones LesWu WeilinTripp Ralph A