MAZ

Last update 08 May 2025

Basic Info

Synonyms

MAZ, MAZI, MYC associated zinc finger protein

+ [10]

Introduction

Binds DNA and functions as a transcriptional activator (PubMed:12270922). Binds to two G/A-rich sites, ME1a1 and ME1a2, within the MYC promoter having greater affinity for the former (PubMed:1502157). Also binds to multiple G/C-rich sites within the promoter of the Sp1 family of transcription factors (PubMed:1502157). Binds DNA and functions as a transcriptional activator (PubMed:12270922). Inhibits MAZ isoform 1-mediated transcription (PubMed:12270922). Binds DNA and functions as a transcriptional activator. Transcriptional regulator, potentially with dual roles in transcription initiation and termination.

100 Clinical Results associated with MAZ

100 Translational Medicine associated with MAZ

0 Patents (Medical) associated with MAZ

334

Literatures (Medical) associated with MAZ

01 Dec 2025·Functional & Integrative Genomics

MAZ-mediated LAMA5 transcription activation promotes gastric cancer progression through the STAT3 signaling

Article

Author: Guo, Xiaobo ; Sun, Qinhui ; Xu, Jiazhong ; Zhang, Hongxia ; Liu, Hongjun ; Wang, Yu

Laminin subunit alpha-5 (LAMA5) has been identified as an oncogene in many cancers, while its role and mechanism in gastric cancer (GC) remain to be explored. Here, the influences of LAMA5 knockdown on GC were investigated in vitro and in vivo. LAMA5 expression was silenced in GC cells alone or in combination with the signal transducer and activator of transcription 3 (STAT3) activator Colivelin, followed by CCK-8, colony formation, EdU, flow cytometry, wound healing assay, and Transwell assay. The regulatory relationship between Myc-associated zinc finger protein (MAZ) and LAMA5 was characterized by ChIP and luciferase reporter analysis. The effect of knockdown of MAZ alone or in combination with LAMA5 overexpression on GC was investigated in vitro and in vivo. LAMA5 was highly expressed in GC cells, and knockdown of LAMA5 inhibited GC cell malignant aggressiveness, which was reversed by the Colivelin treatment. The transcription factor MAZ bound to the promoter of LAMA5 to activate its transcription, and the anti-tumor effects of sh-MAZ on GC cells in vitro and in vivo were overturned by LAMA5 overexpression. In conclusion, MAZ promotes GC cell proliferation and migration by the LAMA5/STAT3 axis, implying that this axis can function as a target for GC therapy.

01 Dec 2025·Functional & Integrative Genomics

Transcription factor MAZ activates the transcription of hypomethylated TYMP in ccRCC

Article

Author: Wang, Yong ; Dong, Yihan ; Li, Jiaxin ; Yue, Dan ; Wang, Rui ; Liu, Xinyu ; Jiang, Huamao ; Lin, Tianyu

Clear cell renal cell carcinoma (ccRCC) is a highly malignant tumor characterized by a significant propensity for recurrence and metastasis. DNA methylation has emerged as a critical epigenetic mechanism with substantial utility in cancer diagnosis. In this study, multi-omics data were utilized to investigate the target genes regulated by the transcription factor MYC-associated zinc finger protein (MAZ) in ccRCC, leading to the identification of thymidine phosphorylase (TYMP) as a gene with notably elevated expression in ccRCC. The interaction between MAZ and TYMP was confirmed through chromatin immunoprecipitation (ChIP) assays and bioinformatics analysis. It was found that the binding of MAZ to the TYMP promoter is associated with the methylation status of this promoter region. Furthermore, the methylation of the TYMP promoter appears to be correlated with both the clinicopathological stage and overall survival of ccRCC patients. Further exploration of genes within the "nucleotide metabolism" pathway, identified through Gene Ontology (GO) enrichment analysis, revealed that uridine phosphorylase 1 (UPP1) interacts with TYMP. Interestingly, UPP1 was also shown to be activated by MAZ, suggesting a coordinated regulatory mechanism. Based on these findings, we propose that the TYMP-UPP1 complex, co-regulated by MAZ, plays a pivotal role in nucleotide metabolism in ccRCC. These results suggest that TYMP may contribute to the pathophysiology of ccRCC and that promoter methylation offers potential as a prognostic indicator, providing novel insights into the molecular underpinnings of ccRCC and potential avenues for therapeutic intervention.

01 May 2025·International Journal of Biological Macromolecules

MAZ-induced lncRNA H19 regulates proliferation and differentiation of porcine skeletal muscle satellite cells via sponge miR-935/miR-296-5p and the p38 MAPK pathway

Article

Author: Fu, Chong ; Liu, Quan ; Li, Mengxun ; Han, Min ; Xie, Su ; Zhou, Honghong ; Li, Changchun

Skeletal muscle satellite cell proliferation and differentiation are important stages in skeletal muscle development, and long non-coding RNAs (lncRNAs) play important roles in both stages. We previously determined the basal functions of lncRNA H19 (H19) and the drebrin 1 (DBN1) gene in porcine skeletal muscle satellite cells (PSCs). However, the mechanisms for H19 and DBN1 regulation of the proliferation and differentiation of PSCs are still unclear. In this study, double luciferase report and pull down results confirmed H19 upregulates DBN1 expression by acting as a miR-935/miR-296-5p decoy. The western blotting results showed upregulated DBN expression activates the p38 mitogen-activated protein kinase (MAPK) pathway to inhibit PSC proliferation and promote differentiation. Moreover, ChIP results showed H19 transcription is regulated by the upstream transcription factor myc-associated zinc finger protein (MAZ). In conclusion, we resolved the mechanism for H19 regulation of proliferation and differentiation of PSCs, contributing to a deeper understanding of the epigenetic regulation of skeletal muscle development and will accelerate advancements in animal genetic improvement.

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