ZNF281

Last update 08 May 2025

Basic Info

Synonyms

GC-box-binding zinc finger protein 1, GZP1, Transcription factor ZBP-99

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Introduction

Transcription repressor that plays a role in regulation of embryonic stem cells (ESCs) differentiation. Required for ESCs differentiation and acts by mediating autorepression of NANOG in ESCs: binds to the NANOG promoter and promotes association of NANOG protein to its own promoter and recruits the NuRD complex, which deacetylates histones. Not required for establishement and maintenance of ESCs (By similarity). Represses the transcription of a number of genes including GAST, ODC1 and VIM. Binds to the G-rich box in the enhancer region of these genes.

100 Clinical Results associated with ZNF281

100 Translational Medicine associated with ZNF281

0 Patents (Medical) associated with ZNF281

Literatures (Medical) associated with ZNF281

01 Apr 2025·International Dental Journal

The Predictive Value of BUB1 in the Prognosis of Oral Squamous Cell Carcinoma

Article

Author: Li, Xiaoqian

BACKGROUNDOral squamous cell carcinoma (OSCC) is the most common type of malignant tumour in the oral cavity, and it is known for its poor prognosis. Budding uninhibited by benzimidazoles 1 (BUB1) may be related to cancer prognosis; however, the specific relationship between BUB1 and OSCC prognosis remains largely unexplored.METHODSThe mRNA levels of BUB1 were analysed using data from the TCGA_OSCC and GSE23558 cohorts. OSCC samples from the TCGA_OSCC dataset were divided into low- and high-BUB1 expression groups based on the median BUB1 level. Furthermore, results of survival analysis, tumour mutation burden (TMB), gene set enrichment analysis (GSEA) pathways, and drug-sensitivity analysis were compared between the 2 groups.RESULTSBased on the data from the TCGA_OSCC and GSE23558 cohorts, BUB1 mRNA levels were significantly upregulated in OSCC tissues compared to healthy controls. Moreover, high expression of BUB1 may serve as an independent indicator of poor prognosis in OSCC. Additionally, patients with high BUB1 expression also exhibited increased levels of immune checkpoints and TMB, suggesting that patients with high BUB1 expression may benefit from immunotherapy. Mechanistically, transcription factors ZFP64, TCF3, and ZNF281 were found to potentially bind to the promoter region of BUB1, thereby regulating its gene expression. Furthermore, GSEA results showed that BUB1 expression was closely related to cell cycle and tumour-related pathways in OSCC. Drug-sensitivity analysis showed that patients with high BUB1 expression may be more sensitive to gemcitabine, paclitaxel, or imatinib.CONCLUSIONSCollectively, results demonstrated that high BUB1 levels may be related to a poor prognosis of OSCC, highlighting its potential as a novel prognostic biomarker for OSCC.

01 Jan 2025·International Immunopharmacology

Inhibition of ZFP281/ZNF281–RIPK1/RIPK3/MLKL signaling in hepatocytes by pterostilbene relieves hepatic lipometabolic disorder and inflammation in non-alcoholic steatohepatitis

Article

Author: Wang, Yang ; Bao, Xiaofeng ; Han, Yiwen ; Wei, Wei ; Wang, Tianle ; Tong, Ye ; Miao, Jingrong ; Lu, Chunfeng ; Zhang, Yu ; Li, Yuanyuan

Non-alcoholic steatohepatitis (NASH) is the most common cause of chronic liver diseases with its pathophysiological mechanism poorly understood. In this work, serological, histological, molecular biological, biochemical, and immunological methods were applied to explore the pathological significance and action of zinc finger protein 281 (ZFP281 in mouse, ZNF281 in human) and targeted strategies. We reported that ZFP281/ZNF281 abundance in hepatocytes was positively correlated with the progression of NASH. Hepatocyte-specific knockdown of Zfp281 prevented mice from NASH diet-induced liver injury, steatosis, inflammation, and fibrosis. Consistently, the metabolic syndromes in NASH mice, characterized by obesity, hyperglycemia, insulin resistance, and hyperlipidemia, were also relieved by hepatocyte-specific Zfp281 deficiency. Mechanistically, incremental ZNF281 led to the upregulation of proinflammatory signaling, receptor-interacting protein kinase 1 (RIPK1)/RIPK3/mixed lineage kinase domain like pseudokinase (MLKL) axis in hepatocytes bearing free fatty acid stress. Activated MLKL translocated to the mitochondrial membrane, disrupting mitochondrial fatty acid β-oxidation and facilitating lipid accumulation in hepatocytes exposed to free fatty acid stimulation; also, MLKL in activated form orientated to the plasma membrane, triggering the lytic death mode in hepatocytes and launching hepatocellular proinflammatory responses. Moreover, we screened a ZFP281 inhibitor, pterostilbene, and demonstrated that pterostilbene, by inhibiting ZFP281 elevation in NASH livers, reduced hepatocyte injury, steatosis, inflammatory responses and fibrogenesis. In conclusion, this work proposes that induction of ZFP281/ZNF281-RIPK1/RIPK3/MLKL signaling disrupts fatty acid metabolism, promoting lipid accumulation, and triggers proinflammatory cell death, accelerating hepatic necroinflammation. Our work identifies ZFP281/ZNF281 as a promising target as well as pterostilbene as a potential strategy for NASH managing.

01 Dec 2024·Aging Cell

Comparative single‐cell transcriptomic analysis across tissues of aging primates reveals specific autologous activation of ZNF281 to mitigate oxidative stress in cornea

Article

Author: Xiao, Yuhua ; Liu, Xu ; Zhong, Jiawei ; Dai, Wangxuan ; Chen, Jia ; Zhang, Shuyao ; Chen, Xu ; Hu, Xing ; Chen, Zheyao ; Hu, Youjin ; Liang, Lingyi

AbstractReactive oxygen species (ROS) and oxidative stress accelerate cellular aging, but their impact on different tissues varies. The cornea, known for its robust antioxidant defense systems, is relatively resistant to age‐related diseases like cancer. However, the precise mechanisms by which the cornea maintains ROS homeostasis during aging remain unclear. Through comparative single‐cell transcriptomic analysis of the cornea and other tissues in young and old nonhuman primates, we identified that a ZNF281 coding transcriptomic program is specifically activated in cornea during aging. Further investigation revealed that ZNF281 forms a positive feedback loop with FOXO3 to sense elevated levels of ROS and mitigate their effects potentially by regulating the mitochondrial respiratory chain and superoxide dismutase (SOD) expression. Importantly, we observed that overexpression of ZNF281 in MSCs prevented cellular senescence. In summary, these findings open up possibilities for understanding tissue‐specific aging and developing new therapies targeting ROS damage.

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ZNF281

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