Ask about this productRelated genes to: ZMAT2 protein
- Gene:
- ZMAT2 NIH gene
- Name:
- zinc finger matrin-type 2
- Previous symbol:
- -
- Synonyms:
- FLJ31121, hSNU23, Snu23
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-06
- Date modifiied:
- 2019-03-21
Related products to: ZMAT2 protein
Related articles to: ZMAT2 protein
- Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition characterized by severe inflammation, immune dysregulation, and oxidative stress, leading to high mortality (30-40%). This study explores the involvement of MAM-related genes in ARDS pathogenesis through bioinformatics and experimental validation. Publicly available RNA-sequencing data from ARDS and control samples were analyzed to identify differentially expressed genes (DEGs). Functional enrichment, gene set variation analysis (GSVA), and weighted gene co-expression network analysis (WGCNA) were performed to explore pathway alterations and hub gene interactions. Immune cell infiltration analysis was conducted using CIBERSORT. Candidate MAM-related genes were validated in a Poly I: C-induced ARDS mouse model and MLE-12 murine lung epithelial cells. The mouse model was assessed for lung histopathology, wet-to-dry lung weight ratio, bronchoalveolar lavage fluid (BALF) inflammatory cytokine levels (IL-1β and TNF-α), and lung injury scores. MLE-12 cells were treated with Poly I: C, and cell viability, lactate dehydrogenase (LDH) release, and apoptosis were evaluated. Protein-protein interaction (PPI) network analysis and drug prediction were used to identify potential therapeutic targets. A total of 3152 DEGs including 1549 upregulated and 1603 downregulated were identified in ARDS samples. Pathway analysis revealed autophagy suppression and immune activation, with 14 immune cell types significantly elevated in ARDS patients. Experimental validation confirmed that Poly I: C-induced ARDS mice exhibited severe lung injury and increased inflammatory reaction, while Poly I: C-treated MLE-12 cells showed increased cytotoxicity and LDH release. ZMAT2 and HBB were identified as key MAM-related hub genes, with ZMAT2 positively associated with disease progression and HBB negatively correlating with lung injury severity. Drug prediction analysis identified 29 pharmacological agents interacting with HBB, suggesting therapeutic potential. This study identifies ZMAT2 and HBB as key MAM-related genes contributing to ARDS pathogenesis, with potential diagnostic and therapeutic applications. The integration of bioinformatics with in vivo and in vitro validation provides novel insights into ARDS molecular mechanisms. Further clinical studies are needed to explore their translational relevance. - Source: PubMed
Publication date: 2025/07/09
Zhou YanqiongChen QiuyingWang XiaoxiaLv KaiminHuang HuiFeng JifengLuo Bijun - Dysregulation of splicing factor expression plays a crucial role in the progression of hepatocellular carcinoma (HCC). Our research found that the expression level of splicing factor ZMAT2 was increased in HCC, promoting the proliferation of HCC cells. RNAseq data indicated that the absence of ZMAT2 induced skipping exon of mRNA, while RIPseq data further revealed the mRNA binding motifs of ZMAT2. A comprehensive analysis of RNAseq and RIPseq data indicateed that ZMAT2 played a crucial role in the maturation process of TRIM28 mRNA. Knocking down of ZMAT2 led to the deletion of 25 bases in exon 11 of TRIM28, ultimately resulting in nonsense-mediated decay (NMD). Our data revealed that ZMAT2 could regulate TRIM28 to reduce the accumulation of ROS in HCC cells, thereby promoting their proliferation. Our research also discovered that ZMAT2 was capable of undergoing phase separation, resulting in the formation of liquid droplet condensates within HCC cells. Additionally, it was found that ZMAT2 was able to form protein-nucleic acid condensates with TRIM28 mRNA. In summary, this study is the first to reveal that ZMAT2 and TRIM28 mRNA form protein-nucleic acid condensates, thereby regulating the splicing of TRIM28 mRNA. The increased expression of ZMAT2 in HCC leads to upregulated TRIM28 expression and reduced ROS accumulation, ultimately accelerating the proliferation of HCC cells. - Source: PubMed
Publication date: 2024/08/20
Zhu YaningLi JiongLi SangYang ZheQiao ZhengkangGu XingshiHe ZhenhuWu DiMa XiaoqianYao ShanhuYang CejunYang MinCao LuZhang JuanWang WeiRong Pengfei - Depression is the most prevalent mental disorder with substantial morbidity and mortality. Although genome-wide association studies (GWASs) have identified multiple risk variants for depression, due to the complicated gene regulatory mechanisms and complexity of linkage disequilibrium (LD), the biological mechanisms by which the risk variants exert their effects on depression remain largely unknown. Here, we perform a transcriptome-wide association study (TWAS) of depression by integrating GWAS summary statistics from 807,553 individuals (246,363 depression cases and 561,190 controls) and summary-level gene-expression data (from the dorsolateral prefrontal cortex (DLPFC) of 1003 individuals). We identified 53 transcriptome-wide significant (TWS) risk genes for depression, of which 23 genes were not implicated in risk loci of the original GWAS. Seven out of 53 risk genes (B3GALTL, FADS1, TCTEX1D1, XPNPEP3, ZMAT2, ZNF501 and ZNF502) showed TWS associations with depression in two independent brain expression quantitative loci (eQTL) datasets, suggesting that these genes may represent promising candidates. We further conducted conditional analyses and identified the potential risk genes that driven the TWAS association signal in each locus. Finally, pathway enrichment analysis revealed biologically pathways relevant to depression. Our study identified new depression risk genes whose expression dysregulation may play a role in depression. More importantly, we translated the GWAS associations into risk genes and relevant pathways. Further mechanistic study and functional characterization of the TWS depression risk genes will facilitate the diagnostics and therapeutics for depression. - Source: PubMed
Publication date: 2021/05/21
Li XiaoyanSu XiLiu JieweiLi HuijuanLi Ming Li WenqiangLuo Xiong-Jian - There has been a considerable concern about cancer induction in response to radiation exposure. However, only a limited number of studies have focused on the biological effects of below-background radiation (BBR) in deep underground environments. To improve our understanding of the effects of BBR on cancer, we studied its biological impact on well-differentiated laryngeal squamous cell carcinoma cells (FD-LSC-1) in a deep underground laboratory (DUGL). The growth curve, morphological, and quantitative proteomic experiments were performed on FD-LSC-1 cells cultured in the DUGL and above-ground laboratory (AGL). The proliferation of FD-LSC-1 cells from the DUGL group was delayed compared to that of cells from the AGL group. Transmission electron microscopy scans of the cells from the DUGL group indicated the presence of hypertrophic endoplasmic reticulum (ER) and a higher number of ER. At a cutoff of absolute fold change ≥ 1.2 and < 0.05, 807 differentially abundant proteins (DAPs; 536 upregulated proteins and 271 downregulated proteins in the cells cultured in the DUGL) were detected. KEGG pathway analysis of these DAPs revealed that seven pathways were enriched. These included ribosome ( < 0.0001), spliceosome ( = 0.0001), oxidative phosphorylation ( = 0.0001), protein export ( = 0.0001), thermogenesis ( = 0.0003), protein processing in the endoplasmic reticulum ( = 0.0108), and non-alcoholic fatty liver disease ( = 0.0421). The BBR environment inhibited the proliferation of FD-LSC-1 cells. Additionally, it induced changes in protein expression associated with the ribosome, gene spliceosome, RNA transport, and energy metabolism among others. The changes in protein expression might form the molecular basis for proliferation inhibition and enhanced survivability of cells adapting to BBR exposure in a deep underground environment. RPL26, RPS27, ZMAT2, PRPF40A, SNRPD2, SLU7, SRSF5, SRSF3, SNRPF, WFS1, STT3B, CANX, ERP29, HSPA5, COX6B1, UQCRH, and ATP6V1G1 were the core proteins associated with the BBR stress response in cells. - Source: PubMed
Publication date: 2020/10/30
Liu JifengMa TengfeiGao MingzhongLiu YilinLiu JunWang ShichaoXie YikeWen QiaoWang LingCheng JuanLiu ShixiZou JianWu JiangLi WeiminXie Heping - Recent advances in genetics present unique opportunities for enhancing our understanding of human physiology and disease predisposition through detailed analysis of gene structure, expression, and population variation via examination of data in publicly accessible genome and gene expression repositories. Yet, the vast majority of human genes remain understudied. Here, we show the scope of these genomic and genetic resources by evaluating , a member of a 5-gene family that through May 2020 had been the focus of only 4 peer-reviewed scientific publications. Using analysis of information extracted from public databases, we show that human is a 6-exon gene and find that it exhibits minimal genetic variation in human populations and in disease states, including cancer. We further demonstrate that the gene and its encoded protein are highly conserved among nonhuman primates and define a cohort of pseudogenes in the marmoset genome. Collectively, our investigations illustrate how complementary use of genomic, gene expression, and population genetic resources can lead to new insights about human and mammalian biology and evolution, and when coupled with data supporting key roles for ZMAT2 in keratinocyte differentiation and pre-RNA splicing argue that this gene is worthy of further study. - Source: PubMed
Publication date: 2020/09/02
Baral KabitaRotwein Peter