Ask about this productRelated genes to: ZNF593 antibody
- Gene:
- ZNF593 NIH gene
- Name:
- zinc finger protein 593
- Previous symbol:
- -
- Synonyms:
- ZT86
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-27
- Date modifiied:
- 2016-10-05
Related products to: ZNF593 antibody
Related articles to: ZNF593 antibody
- The enzyme cyclic GMP-AMP synthase (cGAS) is essential for detecting aberrantly located double-stranded DNA (dsDNA) from genomic, mitochondrial, and microbial origins. Through the synthesis of 2'3'-cGAMP, cGAS triggers the activation of the stimulator of interferon genes pathway, which initiates in vivo innate immune responses. Here, we identify zinc finger proteins ZNF593, which translocate from the nucleus to the cytoplasm after viral infection, as a negative regulator of antiviral type I IFN (IFN-I) production. ZNF593 directly binds to cGAS and suppresses its activation by inhibiting the cGAS-dsDNA interaction. ZNF593 deficiency increases IRF3 nuclear translocation and promotes DNA virus-triggered IFN production. Furthermore, ZNF593 deficiency promotes antiviral innate responses in vivo, improving survival rates in mice against HSV-1 infection. We further find that ZNF593 plays a protective role in systemic lupus erythematosus (SLE) pathology. Notably, replenishing ZNF593 effectively reduced IFN production in peripheral blood mononuclear cells (PBMCs) of SLE patients or in the TMPD-induced murine SLE model. Our findings suggest that ZNF593 negatively regulates IFN-β signaling by targeting cGAS activation, providing new insights into the regulatory mechanisms for antiviral defenses and autoimmune diseases. - Source: PubMed
Publication date: 2025/04/10
Bai XuemeiDong NaCao NanZhou MinYuan JiahuaZhang YulingLiu YaxingZhang JiaJiaChen TianLiu FengSun WanweiZheng YiZhao WeiShu QiangGao ChengjiangLiu Bingyu - Breast cancer, a common malignancy and top cause of female cancer deaths globally, urgently requires new biomarkers and insights into its progression and chemoresistance. In this study, we identify ZNF593, a member of the zinc finger protein family, as an understudied oncogene in breast cancer. ZNF593 is significantly upregulated in breast cancer tissues compared to adjacent normal tissues, which is linked to poor prognosis and advanced clinicopathological features. experiments demonstrate that ZNF593 enhances the proliferation and migration capabilities of breast cancer cells. Comprehensive analyses reveal that ZNF593 is associated with DNA damage repair, cell-cycle regulation, and immunity-related pathways. Mechanistically, ZNF593 protects DNA repair and influences sensitivity to the associated chemotherapy. Furthermore, ZNF593 modulates CCND1, CCNE1, and CCNA2, genes encoding cyclins that facilitate the G1/S transition, resulting in cell-cycle progression. Collectively, our findings identify ZNF593 as a potential therapeutic target for breast cancer, affecting progression and chemoresistance. - Source: PubMed
Publication date: 2024/12/03
Zhang YingfanTang XiaowenWang ChenxinWang MozhiLi MengLi XiangYao LitongXu Yingying - lncRNA ZNF593 antisense (ZNF593-AS) transcripts have been implicated in heart failure through the regulation of myocardial contractility. The decreased transcriptional activity of ZNF593-AS has also been detected in cardiac hypertrophy. However, the function of ZNF593-AS in cardiac hypertrophy remains unclear. Herein, we report that the expression of ZNF593-AS reduced in a mouse model of left ventricular hypertrophy and cardiomyocytes in response to treatment with the hypertrophic agonist phenylephrine (PE). In vivo, ZNF593-AS aggravated pressure overload-induced cardiac hypertrophy in knockout mice. By contrast, cardiomyocyte-specific transgenic mice (ZNF593-AS MHC-Tg) exhibited attenuated TAC-induced cardiac hypertrophy. In vitro, vector-based overexpression using murine or human ZNF593-AS alleviated PE-induced myocyte hypertrophy, whereas GapmeR-induced inhibition aggravated hypertrophic phenotypes. By using RNA-seq and gene set enrichment analyses, we identified a link between ZNF593-AS and oxidative phosphorylation and found that mitofusin 2 (Mfn2) is a direct target of ZNF593-AS. ZNF593-AS exerts an antihypertrophic effect by upregulating Mfn2 expression and improving mitochondrial function. Therefore, it represents a promising therapeutic target for combating pathological cardiac remodeling. - Source: PubMed
Publication date: 2024/05/14
Nie XiangFan JiahuiWang YanwenXie RongChen ChenLi HuapingWang Dao Wen - The ZFX transcriptional activator binds to CpG island promoters, with a major peak at ∼200-250 bp downstream from transcription start sites. Because ZFX binds within the transcribed region, we investigated whether it regulates transcriptional elongation. We used GRO-seq to show that loss or reduction of ZFX increased Pol2 pausing at ZFX-regulated promoters. To further investigate the mechanisms by which ZFX regulates transcription, we determined regions of the protein needed for transactivation and for recruitment to the chromatin. Interestingly, although ZFX has 13 grouped zinc fingers, deletion of the first 11 fingers produces a protein that can still bind to chromatin and activate transcription. We next used TurboID-MS to detect ZFX-interacting proteins, identifying ZNF593, as well as proteins that interact with the N-terminal transactivation domain (which included histone modifying proteins), and proteins that interact with ZFX when it is bound to the chromatin (which included TAFs and other histone modifying proteins). Our studies support a model in which ZFX enhances elongation at target promoters by recruiting H4 acetylation complexes and reducing pausing. - Source: PubMed
Hsu EmilyHutchison KatherineLiu YaoNicolet Charles MSchreiner ShannonZemke Nathan RFarnham Peggy J - Diabetes could directly induce cardiac injury, leading to cardiomyopathy. However, treatment strategies for diabetic cardiomyopathy remain limited. ZNF593-AS knockout and cardiomyocyte-specific transgenic mice were constructed. In addition, high-fat diet (HFD)-induced diabetic mouse model and db/db mice, another classic diabetic mouse model, were employed. ZNF593-AS was silenced using GapmeR, a modified antisense oligonucleotide, while overexpressed using a recombinant adeno-associated virus serotype 9-mediated gene delivery system. Transcriptome sequencing, RNA pull-down assays, and RNA immunoprecipitation assays were also performed to investigate the underlying mechanisms. ZNF593-AS expression was decreased in diabetic hearts. ZNF593-AS attenuated the palmitic acid-induced apoptosis of cardiomyocytes . In HFD-induced diabetic mice, ZNF593-AS deletion aggravated cardiac dysfunction and enhanced cardiac apoptosis and inflammation. In contrast, HFD-induced cardiac dysfunction was improved in ZNF593-AS transgenic mice. Consistently, ZNF593-AS exerted the same cardioprotective effects in db/db mice. Mechanistically, ZNF593-AS directly interacted with the functional domain of interferon regulatory factor 3 (IRF3), and suppressed fatty acid-induced phosphorylation and activation of IRF3, contributing to the amelioration of cardiac cell death and inflammation. In conclusion, our results identified the protective role of ZNF593-AS in diabetic cardiomyopathy, suggesting a novel potential therapeutic target. - Source: PubMed
Publication date: 2023/05/05
Xie RongFan JiahuiWen JianpeiJin KunyingZhan JiabingYuan ShuaiTang YuyanNie XiangWen ZhengLi HuapingChen ChenWang Dao Wen