N6-Methyladenine
(Synonyms: 6-(甲氨基)嘌呤) 目录号 : GC40496
A modified purine of microbial genomes
Cas No.:443-72-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N6-Methyladenine is a modified purine that is commonly found in genomes of prokaryotes, protists, and plants. It is less common in higher eukaryotes and extremely rare in mammals. Like methylation of other DNA residues, N6-methyladenine represents an epigenetic modification that can affect diverse DNA functions, including replication, repair, and expression.
| Cas No. | 443-72-1 | SDF | |
| 别名 | 6-(甲氨基)嘌呤 | ||
| Canonical SMILES | CNC(NC=N1)=C2C1=NC=N2 | ||
| 分子式 | C6H7N5 | 分子量 | 149.2 |
| 溶解度 | DMF: 2 mg/ml,DMSO: 1 mg/ml,Ethanol: 5 mg/ml,PBS (pH 7.2): 2 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.7024 mL | 33.5121 mL | 67.0241 mL |
| 5 mM | 1.3405 mL | 6.7024 mL | 13.4048 mL |
| 10 mM | 0.6702 mL | 3.3512 mL | 6.7024 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
ALKBH1-demethylated DNA N6-Methyladenine modification triggers vascular calcification via osteogenic reprogramming in chronic kidney disease
J Clin Invest 2021 Jul 15;131(14):e146985.PMID:34003800DOI:10.1172/JCI146985.
Vascular calcification (VC) predicts cardiovascular morbidity and mortality in chronic kidney disease (CKD). To date, the underlying mechanisms remain unclear. We detected leukocyte DNA N6-Methyladenine (6mA) levels in patients with CKD with or without aortic arch calcification. We used arteries from CKD mice infected with vascular smooth muscle cell-targeted (VSMC-targeted) adeno-associated virus encoding alkB homolog 1 (Alkbh1) gene or Alkbh1 shRNA to evaluate features of calcification. We identified that leukocyte 6mA levels were significantly reduced as the severity of VC increased in patients with CKD. Decreased 6mA demethylation resulted from the upregulation of ALKBH1. Here, ALKBH1 overexpression aggravated whereas its depletion blunted VC progression and osteogenic reprogramming in vivo and in vitro. Mechanistically, ALKBH1-demethylated DNA 6mA modification could facilitate the binding of octamer-binding transcription factor 4 (Oct4) to bone morphogenetic protein 2 (BMP2) promoter and activate BMP2 transcription. This resulted in osteogenic reprogramming of VSMCs and subsequent VC progression. Either BMP2 or Oct4 depletion alleviated the procalcifying effects of ALKBH1. This suggests that targeting ALKBH1 might be a therapeutic method to reduce the burden of VC in CKD.
DNA N6-Methyladenine Modification in Eukaryotic Genome
Front Genet 2022 Jun 24;13:914404.PMID:35812743DOI:10.3389/fgene.2022.914404.
DNA methylation is treated as an important epigenetic mark in various biological activities. In the past, a large number of articles focused on 5 mC while lacking attention to N6-Methyladenine (6 mA). The presence of 6 mA modification was previously discovered only in prokaryotes. Recently, with the development of detection technologies, 6 mA has been found in several eukaryotes, including protozoans, metazoans, plants, and fungi. The importance of 6 mA in prokaryotes and single-celled eukaryotes has been widely accepted. However, due to the incredibly low density of 6 mA and restrictions on detection technologies, the prevalence of 6 mA and its role in biological processes in eukaryotic organisms are highly debated. In this review, we first summarize the advantages and disadvantages of 6 mA detection methods. Then, we conclude existing reports on the prevalence of 6 mA in eukaryotic organisms. Next, we highlight possible methyltransferases, demethylases, and the recognition proteins of 6 mA. In addition, we summarize the functions of 6 mA in eukaryotes. Last but not least, we summarize our point of view and put forward the problems that need further research.
N6-Methyladenine RNA modification and cancer
Oncol Lett 2020 Aug;20(2):1504-1512.PMID:32724392DOI:10.3892/ol.2020.11739.
N6-methyladenosine (m6A) in messenger RNA (mRNA) is regulated by m6A methyltransferases and demethylases. Modifications of m6A are dynamic and reversible, may regulate gene expression levels and serve vital roles in numerous life processes, such as cell cycle regulation, cell fate decision and cell differentiation. In recent years, m6A modifications have been reported to exhibit functions in human cancers via regulation of RNA stability, microRNA processing, mRNA splicing and mRNA translation, including lung cancer, breast tumor and acute myeloid leukemia. In the present review, the roles of m6A modifications in the onset and progression of cancer were summarized. These modifications display an oncogenic role in certain types of cancer, whereas in other types of cancer they exhibit a tumor suppressor role. Therefore, understanding the biological functions performed by m6A in different types of tumors and identifying pivotal m6A target genes to deduce the potential mechanisms underlying the progression of cancer may assist in the development of novel therapeutics.
N6-Methyladenine DNA modification in Drosophila
Cell 2015 May 7;161(4):893-906.PMID:25936838DOI:10.1016/j.cell.2015.04.018.
DNA N(6)-methyladenine (6mA) modification is commonly found in microbial genomes and plays important functions in regulating numerous biological processes in bacteria. However, whether 6mA occurs and what its potential roles are in higher-eukaryote cells remain unknown. Here, we show that 6mA is present in Drosophila genome and that the 6mA modification is dynamic and is regulated by the Drosophila Tet homolog, DNA 6mA demethylase (DMAD), during embryogenesis. Importantly, our biochemical assays demonstrate that DMAD directly catalyzes 6mA demethylation in vitro. Further genetic and sequencing analyses reveal that DMAD is essential for development and that DMAD removes 6mA primarily from transposon regions, which correlates with transposon suppression in Drosophila ovary. Collectively, we uncover a DNA modification in Drosophila and describe a potential role of the DMAD-6mA regulatory axis in controlling development in higher eukaryotes.
N6-Methyladenine modification in noncoding RNAs and its function in cancer
Biomark Res 2020 Nov 10;8(1):61.PMID:33292652DOI:10.1186/s40364-020-00244-x.
Non-coding RNAs are the main component of the extensive transcription results of the mammalian genome. They are not transcribed into proteins but play critical roles in regulating multiple biological processes and affecting cancer progression. m6A modification is one of the most abundant internal RNA modification of mammalian cells, and it involves almost all aspects of RNA metabolism. Recent research revealed tight correlations between m6A modification and ncRNAs and indicated the interaction between m6A and ncRNAs act a pivotal part in the development of cancer. The correlation between m6A modification and ncRNAs provides a new perspective for exploring the potential regulatory mechanism of tumor gene expression, and suggest that m6A modification and ncRNAs may be important prognostic markers and therapeutic targets for multiple cancers. In this review, we summarize the potential regulatory mechanisms between m6A methylation and ncRNAs, highlighting how their relationship affects biological functions in cancer.