Ask about this productRelated genes to: N6AMT1 Blocking Peptide
- Gene:
- N6AMT1 NIH gene
- Name:
- N-6 adenine-specific DNA methyltransferase 1
- Previous symbol:
- C21orf127, HEMK2
- Synonyms:
- PRED28, N6AMT, MTQ2
- Chromosome:
- 21q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-15
- Date modifiied:
- 2017-08-08
Related products to: N6AMT1 Blocking Peptide
Related articles to: N6AMT1 Blocking Peptide
- N6-methyladenine (6 mA), the most prevalent DNA modification in mammals and other eukaryotes, regulates DNA mismatch repair, chromosome replication, and transcription. However, its role in adult hippocampal neurogenesis remains unkown. Here we showed that the methyltransferase N6amt1 and 6 mA modification were highly enriched in hippocampal neurons both in vitro and in vivo. Functionally, knockdown of N6amt1 in neural stem cells (NSCs) significantly reduced 6 mA levels, neuronal genesis, and proliferation while promoting glial differentiation. Conversely, N6amt1 overexpression enhanced neuronal differentiation and proliferation. Mechanistically, N6amt1-mediated 6 mA modification of Txnrd3 DNA increased its transcription, thereby promoting hippocampal neurogenesis. Furthermore, exogenous Txnrd3 overexpression rescued the defects in cell differentiation and proliferation induced by N6amt1 depletion. Notably, N6amt1 deficiency impaired hippocampal neurogenesis and spatial memory in adult mice. Our findings highlight the critical role of DNA 6 mA in N6amt1-mediated neurogenesis and suggest that targeting N6amt1 may offer a novel therapeutic strategy for neurological disorders associated with cognitive impairment. - Source: PubMed
Publication date: 2025/12/11
Wu YuanfeiMa WenhuiLi QingqingLi YangXie LinjieKong XuejianChen ShuweiWang QianXuan Aiguo - The prognosis of lung adenocarcinoma (LUAD) is poor, and clinical treatment mainly comprises a combination of traditional therapy and immunotherapy. However, the role and mechanism of tumor-infiltrating regulatory T cells (Tregs) in immunotherapy remain controversial. Therefore, we aimed to determine the role of Tregs in LUAD and to construct a relevant prognostic model for future clinical treatment. - Source: PubMed
Publication date: 2025/11/11
Zhao TianYao YanSun YanLv QingliangSun ChanggangCheng YiningGao ChundiZhuang Jing - Imatinib has been widely used in gastrointestinal stromal tumours and significantly improved the prognosis of GIST patients, but approximately half of patients develop acquired treatment resistance, highlighting the urgency for novel therapeutic strategies. - Source: PubMed
Lan JinZhang WeiliZeng KaixuanLi CongHe JiahuaLi XinyueYang RongChi JunHong ZhigangWang WeifengZhou ChiXiao BinyiFan WenhuaLin JunzhongOu QingjianFang YujingPan ZhizhongPeng JianhongLi WeihaoWu Xiaojun - Mammalian sexual reproduction critically relies on the generation of haploid gametes following a specialized cell division process known as meiosis. Here, we demonstrate that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) plays a crucial role in the progression of meiosis during spermatogenesis, as follows. N6AMT1 was expressed in germ cells throughout the entire process of spermatogenesis, with a peak in mRNA levels in spermatocytes at the prophase I stage of meiosis. Germ cell-specific deletion of N6amt1 in mice resulted in male subfertility as well as a significant reduction in sperm count. Notably, N6amt1-null spermatocytes exhibited meiotic arrest at prophase I and extensive apoptosis. Chromosome spreading assays revealed that N6amt1 loss impaired meiotic sex chromosome inactivation (MSCI) and delayed DNA double-strand break (DSB) repair. Correspondingly, transcriptomic analysis identified a substantial increase in transcript levels for genes mapping to sex chromosomes in N6amt1-null mutants, consistent with disruptions in MSCI. Moreover, N6AMT1 deficiency led to a significant upregulation in the steady-state mRNA levels of genes involved in the p53 pathway and functionally activated p53 signaling. Through integrated analysis of data from single-cell RNA sequencing (RNA-seq) and bulk RNA-seq experiments, we found that knockout of N6amt1 primarily affected the transcriptomic profiles of normal pachytene spermatocytes. Taken together, our findings demonstrate that N6AMT1 is required for quantitatively normal male fertility in mice and involved in the molecular mechanisms for meiotic progression during spermatogenesis, including MSCI and DSB repair. - Source: PubMed
Luo YuruLiu ShuangFang YuanSu HongyuDong JinlingLai BaochangWang ZhenYang JuanZhang DonghongWang Yidong - Approximately 70% of breast cancer (BC) cases are luminal-type (estrogen receptor-positive, ER+), suitable for endocrine therapy with tamoxifen as the most commonly used drug. However, about 30% of these patients develop tamoxifen resistance due to various mechanisms, primarily involving PI3K pathway activation through mutations or unknown pathways. Here, we discover, via bioinformatics analysis and clinical samples, that N6 adenine-specific DNA methyltransferase 1 (N6AMT1) is highly expressed in luminal breast cancer but downregulated in tamoxifen-resistant (TamR) BC cells. ChIP-qPCR and luciferase reporter assays showed that FOXA1 binds to the N6AMT1 promoter and enhances its transcription. In TamR models, FOXA1 and N6AMT1 are downregulated, increasing p110α protein levels (but not mRNA), phospho-AKT levels, and tamoxifen resistance. In vivo, N6AMT1 overexpression enhanced tamoxifen sensitivity, while knockdown reduced it; this sensitivity could be restored with the p110α inhibitor A66. Clinically, decreased N6AMT1 expression correlates with poor prognosis in luminal BC patients. In TamR BC organoids, combining tamoxifen with A66 further reduced growth compared to either treatment alone. Mechanistically, increased p110α levels result from inhibited degradation by E3 ubiquitin ligase NEDD4L. These findings suggest N6AMT1 as a potential luminal breast cancer biomarker and highlight the N6AMT1-p110α pathway as a therapeutic target to sensitize cells to tamoxifen. - Source: PubMed
Publication date: 2024/12/02
Ji LikengChen JiongyuHe LifangZhang FanDeng ZihaoLin JiediaoQi ZhaochangLuo XiGiuliano Armando ECui XiaojiangLin Stanley LiCui Yukun