ZNF593

Last update 08 May 2025

Basic Info

Synonyms

zinc finger protein 593, Zinc finger protein T86, ZNF593

+ [1]

Introduction

Involved in pre-60S ribosomal particles maturation by promoting the nuclear export of the 60S ribosome (PubMed:32669547). Negatively modulates the DNA binding activity of Oct-2 and therefore its transcriptional regulatory activity (PubMed:9115366).

100 Clinical Results associated with ZNF593

100 Translational Medicine associated with ZNF593

0 Patents (Medical) associated with ZNF593

Literatures (Medical) associated with ZNF593

01 Dec 2024·iScience

Zinc finger protein 593 promotes breast cancer development by ensuring DNA damage repair and cell-cycle progression

Article

Author: Wang, Chenxin ; Xu, Yingying ; Wang, Mozhi ; Li, Xiang ; Zhang, Yingfan ; Tang, Xiaowen ; Li, Meng ; Yao, Litong

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. In vitro 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.

08 Jul 2024·Nucleic Acids Research

Reduction of ZFX levels decreases histone H4 acetylation and increases Pol2 pausing at target promoters

Article

Author: Hutchison, Katherine ; Farnham, Peggy J ; Liu, Yao ; Hsu, Emily ; Schreiner, Shannon ; Zemke, Nathan R ; Nicolet, Charles M

AbstractThe 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.

01 Jun 2024·Frontiers of Medicine

lncRNA ZNF593-AS inhibits cardiac hypertrophy and myocardial remodeling by upregulating Mfn2 expression

Article

Author: Li, Huaping ; Chen, Chen ; Wang, Dao Wen ; Nie, Xiang ; Fan, Jiahui ; Wang, Yanwen ; Xie, Rong

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.

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ZNF593

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