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2'-O-Methyladenosine Sale

(Synonyms: 2'-O-甲基腺苷) 目录号 : GC41282

An adenosine analog

2'-O-Methyladenosine Chemical Structure

Cas No.:2140-79-6

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产品描述

2'-O-Methyladenosine is an analog of adenosine used to prepare nucleoside derivatives as inhibitors of viral RNA translation and replication.

Chemical Properties

Cas No. 2140-79-6 SDF
别名 2'-O-甲基腺苷
Canonical SMILES NC1=NC=NC2=C1N=CN2[C@H]3[C@H](OC)[C@H](O)[C@@H](CO)O3
分子式 C11H15N5O4 分子量 281.3
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Research Update

A comprehensive review of m6A/m6Am RNA methyltransferase structures

Nucleic Acids Res 2021 Jul 21;49(13):7239-7255.PMID:34023900DOI:10.1093/nar/gkab378.

Gene expression is regulated at many levels including co- or post-transcriptionally, where chemical modifications are added to RNA on riboses and bases. Expression control via RNA modifications has been termed 'epitranscriptomics' to keep with the related 'epigenomics' for DNA modification. One such RNA modification is the N6-methylation found on adenosine (m6A) and 2'-O-Methyladenosine (m6Am) in most types of RNA. The N6-methylation can affect the fold, stability, degradation and cellular interaction(s) of the modified RNA, implicating it in processes such as splicing, translation, export and decay. The multiple roles played by this modification explains why m6A misregulation is connected to multiple human cancers. The m6A/m6Am writer enzymes are RNA methyltransferases (MTases). Structures are available for functionally characterized m6A RNA MTases from human (m6A mRNA, m6A snRNA, m6A rRNA and m6Am mRNA MTases), zebrafish (m6Am mRNA MTase) and bacteria (m6A rRNA MTase). For each of these MTases, we describe their overall domain organization, the active site architecture and the substrate binding. We identify areas that remain to be investigated, propose yet unexplored routes for structural characterization of MTase:substrate complexes, and highlight common structural elements that should be described for future m6A/m6Am RNA MTase structures.

The 2'-O-Methyladenosine nucleoside modification gene OsTRM13 positively regulates salt stress tolerance in rice

J Exp Bot 2017 Mar 1;68(7):1479-1491.PMID:28369540DOI:10.1093/jxb/erx061.

Stress induces changes of modified nucleosides in tRNA, and these changes can influence codon-anticodon interaction and therefore the translation of target proteins. Certain nucleoside modification genes are associated with regulation of stress tolerance and immune response in plants. In this study, we found a dramatic increase of 2'-O-Methyladenosine (Am) nucleoside in rice seedlings subjected to salt stress and abscisic acid (ABA) treatment. We identified LOC_Os03g61750 (OsTRM13) as a rice candidate methyltransferase for the Am modification. OsTRM13 transcript levels increased significantly upon salt stress and ABA treatment, and the OsTrm13 protein was found to be located primarily to the nucleus. More importantly, OsTRM13 overexpression plants displayed improved salt stress tolerance, and vice versa, OsTRM13 RNA interference (RNAi) plants showed reduced tolerance. Furthermore, OsTRM13 complemented a yeast trm13Δ mutant, deficient in Am synthesis, and the purified OsTrm13 protein catalysed Am nucleoside formation on tRNA-Gly-GCC in vitro. Our results show that OsTRM13, encoding a rice tRNA nucleoside methyltransferase, is an important regulator of salt stress tolerance in rice.

Correction: FTSJ1 regulates tRNA 2'-O-Methyladenosine modification and suppresses the malignancy of NSCLC via inhibiting DRAM1 expression

Cell Death Dis 2020 Jun 3;11(6):418.PMID:32488007DOI:10.1038/s41419-020-2623-9.

The original version of this article contained an error in the spelling of the author Yuchen Chen, which was incorrectly given as Yuhuan Chen. This has now been corrected in both the PDF and HTML versions of the article.

FTSJ1 regulates tRNA 2'-O-Methyladenosine modification and suppresses the malignancy of NSCLC via inhibiting DRAM1 expression

Cell Death Dis 2020 May 11;11(5):348.PMID:32393790DOI:10.1038/s41419-020-2525-x.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. The mechanisms underlying NSCLC tumorigenesis are incompletely understood. Transfer RNA (tRNA) modification is emerging as a novel regulatory mechanism for carcinogenesis. However, the role of tRNA modification in NSCLC remains obscure. In this study, HPLC/MS assay was used to quantify tRNA modification levels in NSCLC tissues and cells. tRNA-modifying enzyme genes were identified by comparative genomics and validated by qRT-PCR analysis. The biological functions of tRNA-modifying gene in NSCLC were investigated in vitro and in vivo. The mechanisms of tRNA-modifying gene in NSCLC were explored by RNA-seq, qRT-PCR, and rescue assays. The results showed that a total of 18 types of tRNA modifications and up to seven tRNA-modifying genes were significantly downregulated in NSCLC tumor tissues compared with that in normal tissues, with the 2'-O-Methyladenosine (Am) modification displaying the lowest level in tumor tissues. Loss- and gain-of-function assays revealed that the amount of Am in tRNAs was significantly associated with expression levels of FTSJ1, which was also downregulated in NSCLC tissues and cells. Upregulation of FTSJ1 inhibited proliferation, migration, and promoted apoptosis of NSCLC cells in vitro. Silencing of FTSJ1 resulted in the opposite effects. In vivo assay confirmed that overexpression of FTSJ1 significantly suppressed the growth of NSCLC cells. Mechanistically, overexpression of FTSJ1 led to a decreased expression of DRAM1. Whereas knockdown of FTSJ1 resulted in an increased expression of DRAM1. Furthermore, silencing of DRAM1 substantially augmented the antitumor effect of FTSJ1 on NSCLC cells. Our findings suggested an important mechanism of tRNA modifications in NSCLC and demonstrated novel roles of FTSJ1 as both tRNA Am modifier and tumor suppressor in NSCLC.

Quantitative Analysis of Methylated Adenosine Modifications Revealed Increased Levels of N 6-Methyladenosine (m6A) and N 6,2'- O-Dimethyladenosine (m6Am) in Serum From Colorectal Cancer and Gastric Cancer Patients

Front Cell Dev Biol 2021 Jul 26;9:694673.PMID:34381776DOI:10.3389/fcell.2021.694673.

Colorectal cancer and gastric cancer are the most prevalent gastrointestinal malignancies worldwide, and early detection of these cancers is crucial to reduce their incidence and mortality. RNA methylation plays an important regulatory role in a variety of physiological activities, and it has drawn great attention in recent years. Methylated adenosine (A) modifications such as N 6-methyladenosine (m6A), N 1-methyladenosine (m1A), 2'-O-Methyladenosine (Am), N 6,2'-O-dimethyladenosine (m6Am), and N 6,N 6-dimethyladenosine (m6 2A) are typical epigenetic markers of RNA, and they are closely correlated to various diseases including cancer. Serum is a valuable source of biofluid for biomarker discovery, and determination of these adenosine modifications in human serum is desirable since they are emerging biomarkers for detection of diseases. In this work, a targeted quantitative analysis method using hydrophilic interaction liquid chromatography-tandem mass spectrometry (HILIC-MS/MS) was developed and utilized to analyze these methylated adenosine modifications in serum samples. The concentration differences between the healthy volunteers and cancer patients were evaluated by Mann-Whitney test, and receiver operator characteristic (ROC) curve analysis was performed to access the potential of these nucleosides as biomarkers. We demonstrated the presence of the m6Am in human serum for the first time, and we successfully quantified the concentrations of A, m6A, m1A, and m6Am in serum samples from 99 healthy controls, 51 colorectal cancer patients, and 27 gastric cancer patients. We found that the levels of m6A and m6Am in serum were both increased in colorectal cancer or gastric cancer patients, compared to that in healthy controls. These results indicate that m6A and m6Am in serum may act as potential biomarkers for early detection and prognosis of colorectal cancer and gastric cancer. In addition, the present work will stimulate investigations on the effects of adenosine methylation on the initiation and progression of colorectal cancer and gastric cancer.