N3-methyl-uridine - CAS 2140-69-4
Product Name:
Catalog Number:
ST056933; 3-methyl-Uridine; AC1L7V2K; SCHEMBL18512961; 1-[3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-3-methylpyrimidine-2,4-dione
CAS Number:
3-Methyluridine is a modified nucleoside of RNA.
Molecular Weight:
Molecular Formula:
Canonical SMILES:
Ribo-Nucleosides | Cancer and Proliferation Marker Nucleosides
Chemical Structure
CAS 2140-69-4 N3-methyl-uridine

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Reference Reading

1.Deoxyuridines from the marine sponge associated actinomycete Streptomyces microflavus.
Li K1, Li QL, Ji NY, Liu B, Zhang W, Cao XP. Mar Drugs. 2011;9(5):690-5. doi: 10.3390/md9050690. Epub 2011 Apr 26.
One new nucleoside derivative, named 3-acetyl-5-methyl-2'-deoxyuridine (1), along with two known compounds 3,5-dimethyl-2'-deoxyuridine (2) and 3-methyl-2'-deoxyuridine (3), were isolated from the cultures of Streptomyces microflavus. This strain was an associated actinomycete isolated from the marine sponge Hymeniacidon perlevis collected from the coast of Dalian (China). Their structures were elucidated by detailed NMR and MS spectroscopic analysis as well as comparison with literature data.
2.Combining nucleoside analogues to achieve recognition of oligopurine tracts by triplex-forming oligonucleotides at physiological pH.
Rusling DA1, Le Strat L, Powers VE, Broughton-Head VJ, Booth J, Lack O, Brown T, Fox KR. FEBS Lett. 2005 Dec 5;579(29):6616-20. Epub 2005 Nov 9.
We have used DNase I footprinting to examine DNA triple helix formation at a 12 base pair oligopurine.oligopyrimidine sequence, using oligonucleotides that contain combinations of 2'-aminoethoxy-5-(3-aminoprop-1-ynyl)uridine (bis-amino-U, BAU) and 3-methyl-2-aminopyridine (MeP) in place of T and C, respectively. This combination acts cooperatively to enable high affinity triple helix formation at physiological pH. The affinity depends on the number of substitutions and their arrangement; oligonucleotides in which these analogues are evenly distributed throughout the third strand bind much better than those in which they are clustered together.
3.A role for Akt in epidermal growth factor-stimulated cell cycle progression in cultured hepatocytes: generation of a hyperproliferative window after adenoviral expression of constitutively active Akt.
Luo Y1, Dixon CJ, Hall JF, White PJ, Boarder MR. J Pharmacol Exp Ther. 2007 Jun;321(3):884-91. Epub 2007 Mar 19.
Epidermal growth factor (EGF) stimulation of cell cycle progression in cultured primary hepatocytes has previously been reported to be dependent on the mammalian target of rapamycin (mTOR) elements of the phosphoinositide 3-kinase (PI3K) signaling cascade and not the Akt pathway. Here we have established conditions of combined treatment of rat hepatocytes with insulin and EGF that favor cell cycle progression. The resulting cell population expresses albumin and retains receptor regulation of the signaling pathways leading to glycogen phosphorylase activation. We then investigated the hypothesis that the Akt limb of the PI3K pathway plays a central role in this insulin/EGF enhancement of cell cycle progression. The phosphorylation of Akt, central to the PI3K pathway, was increased by both insulin (sustained) and EGF (transient). The stimulation of Akt phosphorylation was inhibited in a concentration-dependent manner by the PI3K inhibitor, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002).
4.3-Methyl-4-nitrophenol metabolism by uridine diphosphate glucuronosyltransferase and sulfotransferase in liver microsomes of mice, rats, and
Lee CH1, Kamijima M, Li C, Taneda S, Suzuki AK, Nakajima T. Environ Toxicol Chem. 2007 Sep;26(9):1873-8.
3-Methyl-4-nitrophenol (PNMC) is a component of diesel exhaust particles and one of the major breakdown products of the insecticide fenitrothion. This chemical has a high potential for reproductive toxicity in Japanese quail (Coturnix japonica) and rats. Because PNMC inhaled by the body is metabolized by uridine diphosphate glucuronosyltransferase (UGT) and sulfotransferase, we investigated these enzyme activities in the hepatic microsomes and cytosols of quail (as a model of wild birds) and compared these activities with those of rats and mice as models of ecological and human risk assessment. The maximum velocity of the UGT for PNMC in quail was 12.7 nmol/min/mg, which was one third and one fourth those of rats and mice, respectively. The Michaelis-Menten constant of UGT for PNMC in quail was 0.29 mM, which was 1.3- and 1.8-fold higher than that in mice and rats, respectively, but not significantly different. In accordance with these results, UGT activities for PNMC were lowest in quail, with those in mice and rats being 4.