NMN分子结构 NMN词典
中文名称:beta-烟酰胺单核苷酸
中文别名:β-烟酰胺单核苷酸; 烟酰胺核苷酸
英文名称:beta-nicotinamide mononucleotide
英文别名:
3-carbamoyl-1-[5-O-(hydroxyphosphinato)-beta-D-ribofuranosyl]pyridinium;
3-(Aminocarbonyl)-1-(5-O-phosphonato-beta-D-ribofuranosyl)pyridinium;
3-(aminocarbonyl)-1-(5-O-phosphono-beta-D-ribofuranosyl) ;
3-carbamoyl-1-(5-O-phosphonopentofuranosyl)pyridinium; coenzyme NMN;
β-Nicotinamide mononucleotide; Nicotinamide mononucleotide; NMN; inner salt; Pyridinium;
CAS号:1094-61-7
EINECS号:214-136-5
分子式:C11H15N2O8P
分子量:334.2192
InChI:InChI=1/C11H15N2O8P/c12-10(16)6-2-1-3-13(4-6)11-9(15)8(14)7(21-11)5-20-22(17,18)19/h1-4,7-9,11,14-15H,5H2,(H3-,12,16,17,18,19)/t7-,8-,9-,11-/m1/s1
性质描述:其外观呈冷冻干燥粉末状,溶于水。
NMN是NAD+的前体 NAD+又叫辅酶Ⅰ,全称烟酰胺腺嘌呤二核苷酸,又称二磷酸烟苷,存在每一个细胞中参与上千项反应。NAD+是三羧酸循环的重要辅酶,促进糖、脂肪、氨基酸的代谢,参与能量的合成;NAD+又是辅酶I消耗酶的唯一底物(DNA修复酶PARP的唯一底物、长寿蛋白Sirtuins的唯一底物、环ADP核糖合成酶CD38/157的唯一底物)。
引用文献
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3,Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice
4,CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechani **
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6,Resistance Exercise Training Alters Mitochondrial Function in Hu ** nSkeletal Muscle
7,Pathways and subcellular compartmentation of NADbiosynthesis in hu ** n cells: from entry of extracellular precursors tomitochondrial NAD generation.
8,Loss of NAD Homeostasis Leads to Progressive andReversible Degeneration of Skeletal Muscle (Fredrick 2016)
9,Digestion andabsorption of NAD by the s ** ll intestine of the rat (Henderson, 1983)
10, Effects of a widerange of ** tary nicotinamide riboside (NR) concentrations on metabolicflexibility and white adipose tissue (WAT) of mice fed a mildly obesogenic ** t
11,Nicotinamide Mononucleotide, an NAD+ Precursor, Rescues Age-AssociatedSusceptibility to AKI in a Sirtuin 1-Dependent Manne
12,The NAD+ Precursor Nicotinamide Riboside Enhances OxidativeMetaboli ** and Protects against High-Fat Diet-Induced Obesity
13,Long-Term Administration of Nicotinamide Mononucleotide MitigatesAge-Associated Physiological Decline in Mice.Cell Metaboli ** , v.24, no.6, 2016Dec 13, p.795(12)
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19, A conserved NAD+ binding pocket that regulates protein-proteininteractions during aging
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24, Nicotinamide mononucleotide, a key NAD+ intermediate, treats thepathophysiology of ** t- and age-induced diabetes in mice
25, P7C3 neuroprotective chemicals block axonal degeneration andpreserve function after trau ** tic brain injury. Yin, T.C., Britt, J.K., DeJesús Cortés, H., Lu, Y., Genova, R.M., Khan, M.Z., Voorhees, J.R., Shao, J.,Katz ** n, A.C., Huntington, P.J. et al. Cell Rep. 2014; 8: 1731–1740
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28, NAD+ Replenishment Improves Lifespan and Healthspan in AtaxiaTelangiectasia Models via Mitophagy and DNA Repair Substance with the potentialto postpone aging
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30,Nicotinamide riboside restores cognition through an upregulation ofproliferator activated receptor-γ coactivator 1α regulated β secretase 1degradation and mitochondrial gene expression in Alzheimer’s mouse models.Gong, B., Pan, Y., Vempati, P., Zhao, W., Knable, L., Ho, L., Wang, J., Sastre,M., Ono, K., Sauve, A.A., and Pasinetti, G.M. Neurobiol. Aging. 2013; 34:1581–1588
31,NAD+ and sirtuins in aging and disease (I ** i, 2014)
32,Declining NAD+ Induces a Pseudohypoxic State DisruptingNuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)
33, un Li,Zhenkun Lou, Vera Gorbunova, L. Aravind, Clemens Steegborn, David A. Sinclair.A conserved NAD+ binding pocket that regulates protein-protein interactions duringaging. Science 355:1312,(2017)
34,Mouchiroud L., Houtkooper R.H., Moullan N., et al.. TheNAD+/Sirtuin pathway modulates longevity through activation of mitochondrialUPR and FOXO signaling. Cell 154: 430-441 (2013)
35,Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats thePathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011
36,Head to Head Comparison of Short-Term Treatment with the NAD(+)Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in ObeseFe ** le Mice (Uddin, 2016)
37, Evidence for a direct effect of the NAD+ precursor acipimox onmuscle mitochondrial function in hu ** ns. van de Weijer, T., Phielix, E., Bilet,L., Williams, E.G., Ropelle, E.R., Bierwagen, A., Livingstone, R., Nowotny, P.,Sparks, L.M., Paglialunga, S. et al. Diabetes. 2015; ** : 1193–1201
38,Nicotinamide mononucleotide attenuates brain injury afterintracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway (Wei, 2017)
39,Nicotinamide mononucleotide protects against β-amyloidoligomer-induced cognitive impairment and neuronal death (Wang, 2016)
40,Nicotinamide mononucleotide inhibits JNK activation to reverseAlzheimer disease (Yao, 2017)
41,Nicotinamidemononucleotide, an intermediate of NAD+ synthesis, protects the heart fromischemia and repercussion (Ya ** moto, 2014)
42,Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects theheart from ischemia and repercussion
43,Nicotinamide mononucleotide supplementation reverses vasculardysfunction and oxidative stress with aging in mice (de Picciotto, 2016)
44,Short-ter ** dministration of Nicotinamide Mononucleotide preserves cardiac mitochondrialhomeostasis and prevents heart failure (Zhang, 2017)
45,Nicotinamide mononucleotide requires SIRT3 to improve cardiacfunction and bioenergetics in a Friedreich’s ataxia cardiomyopathy model
46,Samuel W.French. Chronic alcohol binging injures the liver andother organs by reducing NAD⁺ levels required for sirtuin's deacetylaseactivity. Experimental and Molecular Pathology 100:303-306(2016)
47,NAMPT-mediatedNAD+ biosynthesis is essential for vision in mice (lin, 2016)
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