Ask about this productRelated genes to: ZCCHC3 antibody
- Gene:
- ZCCHC3 NIH gene
- Name:
- zinc finger CCHC-type containing 3
- Previous symbol:
- C20orf99
- Synonyms:
- dJ1103G7.7
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-02-12
Related products to: ZCCHC3 antibody
Related articles to: ZCCHC3 antibody
- This study aimed to investigate the role of urocanic acid (UCA) modulates cognitive impairment in a D-galactose (DG)-induced aging model, providing new insights and a theoretical foundation for the treatment of related diseases. Mouse senescence and astrocyte model was created by DG-induced stimuli to assess the effects of UCA. Molecular docking was utilized to confirm potential targets of UCA, and the interaction was validated using the Drug Affinity Responsive Target Stability assay combined with Western blot analysis. The molecular mechanism of UCA was elucidated through in vivo and in vitro experiments. The result showed that UCA treatment ameliorated learning and memory capabilities in DG-induced mice, maintains astrocyte morphology while reducing apoptosis and senescent cells, and inflammatory factors. Additionally, UCA treatment alleviated cell cycle arrest. Molecular docking revealed direct binding between UCA and the ZCCHC3 protein. ZCCHC3 overexpression exacerbated cellular senescence, increased apoptosis and senescent cells, and inflammatory factor levels, while simultaneously activating the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway. UCA treatment reversed the effects of ZCCHC3 overexpression. Mechanistically, UCA inhibited the cGAS/STING pathway by binding to ZCCHC3, thereby alleviating cellular senescence. In vivo experiments further confirmed that ZCCHC3 overexpression or exogenous cGAS activation negated the cognitive protective effects of UCA. The study demonstrates that UCA alleviates cognitive impairment and astrocyte senescence by directly binding to ZCCHC3 to suppress the cGAS‑STING pathway. These results identify ZCCHC3 as a novel therapeutic target and clarify the molecular basis of related disorders.raci. - Source: PubMed
Publication date: 2026/03/26
Hu ShengKou ZhixiongChen BinYang YihanYou Yong - Ovarian cancer is a prevalent gynecological malignancy among women worldwide, with its high rates of recurrence, metastasis, and mortality, underscoring the need to identify reliable prognostic factors. Recent findings have indicated that zinc finger CCHC-type containing 3 (ZCCHC3) and estrogen-responsive finger protein (Efp), which function in anti-RNA virus innate immunity as protein binding partners, are potential prognostic markers in patients with triple-negative breast cancer. Furthermore, a correlation has been observed between Efp immunoreactivity (IR) and advanced disease stage in ovarian carcinomas. However, the pathophysiological role of ZCCHC3 and Efp in ovarian carcinoma remains to be elucidated. We investigated IR of ZCCHC3 and Efp in a cohort of high-grade serous ovarian carcinoma (HGSC) and clear cell ovarian carcinoma (CCC). ZCCHC3 IR was associated with pathological T factor, stage, histological type, Ki67 labeling index, and Efp IR. Positive ZCCHC3 and Efp statuses were each significantly correlated with worse disease-free survival (DFS) in Kaplan-Meier survival analysis. In addition, combined ZCCHC3 and Efp positivity was associated with poor DFS in univariate analysis and showed a trend toward worse survival in multivariate analysis. These findings suggest that ZCCHC3 and Efp play a significant role in HGSC and CCC progression, likely due to their cooperative interactions. - Source: PubMed
Iwabuchi ErinaSuzuki TakashiIkeda KazuhiroShibuya YusukeShigeta ShogoShimada MuneakiHorie KunikoInoue Satoshi - The strategy of viruses targeting RIG-I to disrupt the interferon (IFN) system represents an effective mechanism for evading innate immune responses. In this study, we observed that porcine reproductive and respiratory syndrome virus (PRRSV) GP2a inhibited IFN production by targeting RIG-I. Further studies revealed that GP2a blocks the RIG-I-like receptor signaling pathway through two mechanisms: (i) GP2a induces K48-linked ubiquitination of RIG-I by promoting the interaction between RIG-I and RING finger protein 125 (RNF125), resulting in RIG-I degradation, and (ii) GP2a hijacks zinc finger CCHC-type containing 3 (ZCCHC3) to disrupt the formation of the tripartite motif-containing 25 (TRIM25)-RIG-I complex, thereby inhibiting RIG-I K63-linked ubiquitination. This inhibition effectively prevents the activation and expression of RIG-I. In conclusion, our findings demonstrate novel mechanisms by which PRRSV GP2a inhibits IFN production, thereby improving our understanding of PRRSV immune evasion strategies.IMPORTANCEPorcine reproductive and respiratory syndrome is an important viral disease that affects the swine industry worldwide. PRRSV glycoproteins (GPs) play a crucial role in the viral infection process. However, it remains largely unknown about what roles PRRSV GPs play in antagonizing the innate immune response. In this study, we found that GP2a targets RIG-I to inhibit IFN production through a dual-faceted mechanism. GP2a promotes the RNF125-mediated degradation of RIG-I and competitively interacts with ZCCHC3 to impede TRIM25-induced RIG-I activation. This research contributes to a deeper understanding of the immune escape mechanisms employed by PRRSV. - Source: PubMed
Publication date: 2025/10/10
Xiang YingjieMou ChunxiaoZhao XingZhuo ChenShi KaichuangGo Yun YoungChen Zhenhai - Porcine epidemic diarrhea virus (PEDV) infection in pigs is characterized by vomiting, dehydration, and diarrhoea. The structural proteins of PEDV play crucial roles in viral entry, release, assembly, outgrowth, and host immune regulation. Similar to other viruses, PEDV primarily relies on host cellular mechanisms for productive infection. However, the host factors associated with PEDV infection remain undefined. Therefore, an in-depth understanding of the pathogenic mechanisms of PEDV is essential for comprehending this disease. Zinc-containing finger CCHC-type protein 3 (ZCCHC3) is an antiviral factor known to interact with RIG-I and cGAS, inhibiting the replication of pseudorabies virus (PRV). In this study, we investigated the role of porcine ZCCHC3 in PEDV proliferation. We first demonstrated that the expression of ZCCHC3 in LLC-PK1 cells is downregulated upon PEDV infection. Overexpression of ZCCHC3 inhibited PEDV replication, whereas knockdown of ZCCHC3 increased viral titer and N protein levels. Further studies revealed that ZCCHC3 interacts and co-localizes with N proteins, and that ZCCHC3-mediated antiviral effects depend on its zinc finger protease activity. Taken together, these findings provide valuable insights into the role of ZCCHC3 in PEDV proliferation and enhance our understanding of host-virus interactions. - Source: PubMed
Publication date: 2025/03/06
Zhang ZuyaoWang ShuangyangSun HuihuiLi JieWang JunLi YangfanLin HaichenWang XuanBi RuiminBo ZongyiShen HaixiaoLi LiangSun Pei - In this issue of Molecular Cell, Shi et al. elucidate a novel role of host factor ZCCHC3 in positively regulating RLR and cGAS signaling through the binding of nucleic acids and induction of liquid phase condensation. - Source: PubMed
Barker RebeccaBartok Eva