15763-06-1
15763-06-1
Chemical Structure
1-Methyladenosine
- CAS No.: 15763-06-1
- Formula:C11H15N5O4
- Molecular Weight:281.27
IUPAC Name: (2R,3S,4R,5R)-2-(hydroxymethyl)-5-(6-imino-1-methyl-1,6-dihydro-9H-purin-9-yl)tetrahydrofuran-3,4-diol
InChIKey: GFYLSDSUCHVORB-IOSLPCCCSA-N
SMILES: OC[C@@H]1[C@@H](O)[C@@H](O)[C@H](N2C(N=CN(C)C3=N)=C3N=C2)O1
Biological Activity: 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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1-Methyladenosine | 99.92% | 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis. | ||||||||||||||||||||
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1-Methyladenosine (Standard) | 98.02% | 1-Methyladenosine (Standard) is the analytical standard of 1-Methyladenosine. This product is intended for research and analytical applications. 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis. In Vitro:Compared to surrounding tumor tissues, 1-methyladenosine methylation in RNA is aberrantly elevated in hepatocellular carcinoma (HCC) cell lines and liver cancer stem cells (CSCs). Methylated 1-methyladenosine can promote cholesterol synthesis and activate the Hedgehog signaling pathway by enhancing the translation of PPARδ in liver CSCs, ultimately driving the self-renewal and tumorigenesis of liver cancer stem cells. | ||||||||||||||||||||
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1-Methyladenosine-d3 hydriodide | 99.87% | 1-Methyladenosine-d3 hydriodide is the deuterium labeled 1-Methyladenosine (HY-113081). 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis. | ||||||||||||||||||||
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1-Methyladenosine-d3 | 96.12% | 1-Methyl Adenosine-d3 is the deuterium labeled 1-Methyladenosine. 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis. | ||||||||||||||||||||
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1-Methyladenosine-d3 hydrochloride | 98.05% | 1-Methyladenosine-d3 hydrochloride is the hydrochloride salt form of deuterium labeled 1-Methyladenosine (HY-113081). 1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis. | ||||||||||||||||||||
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References
- [1]. Hauenschild R, et al. The reverse transcription signature of N-1-methyladenosine in RNA-Seq is sequence dependent. Nucleic Acids Res. 2015 Nov 16;43(20):9950-64. [Content Brief]
- [2]. Banys K, et al. Effect of Genistein Supplementation on the Progression of Neoplasms and the Level of the Modified Nucleosides in Rats With Mammary Cancer. In Vivo. 2021 Jul-Aug;35(4):2059-2072. [Content Brief]
- [3]. Wang Y, et al. N 1-methyladenosine methylation in tRNA drives liver tumourigenesis by regulating cholesterol metabolism[J]. Nature communications, 2021, 12(1): 6314. [Content Brief]
