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1 ng enzyme in the NAD(+) salvage pathway from nicotinamide.
2 the response of the circadian oscillator to nicotinamide.
3 hat can be normalized by the anti-aging drug nicotinamide.
4 l (CI), 0.65-3.11]; low certainty evidence), nicotinamide (2 trials, 60 participants), acitretin (2 t
5 f 2,3,4-trihydroxy-5-methylacetophenone (1), nicotinamide (2), and uracil (3) from palmyra palm syrup
8 ment in vivo with the NAD(+) repleting agent nicotinamide, a form of vitamin B3, prevented thymus atr
9 When the diversity search was extended to nicotinamides, a single fluorine atom addition was found
10 the new visualization technique elucidates a nicotinamide accumulation that mirrors that of hypoxanth
11 ine dinucleotide(+) (NAD(+))/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NA
15 enzymes of redox reactions: oxidized/reduced nicotinamide adenine dinucleotide (NAD(+) and NADH) and
16 s an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD(+)) and is a cand
17 yl guanosine (m(7)G) cap, a non-canonical 5' nicotinamide adenine dinucleotide (NAD(+)) cap can tag c
18 ver, mammalian mRNAs can also carry a 5' end nicotinamide adenine dinucleotide (NAD(+)) cap that, in
19 critical step in the de novo biosynthesis of nicotinamide adenine dinucleotide (NAD(+)) in mammals.
23 energy stress and oxidative stress response, nicotinamide adenine dinucleotide (NAD(+)) is emerging a
29 tinamide riboside (NR) is a newly discovered nicotinamide adenine dinucleotide (NAD(+)) precursor vit
30 sferase (NMNAT), an evolutionarily conserved nicotinamide adenine dinucleotide (NAD(+)) synthase and
32 a PTM, in which ADP-ribosyltransferases use nicotinamide adenine dinucleotide (NAD(+)) to modify tar
34 monstrate that cell-autonomous generation of nicotinamide adenine dinucleotide (NAD(+)) via the kynur
36 Nicotinamide (NAM) is the main precursor of nicotinamide adenine dinucleotide (NAD(+)), a coenzyme e
41 ng NAD synthetase 1, the final enzyme of the nicotinamide adenine dinucleotide (NAD) de novo synthesi
42 ing liver regeneration, the concentration of nicotinamide adenine dinucleotide (NAD) falls, at least
45 ation telomerase knockout mice display lower nicotinamide adenine dinucleotide (NAD) levels, and an i
46 be potent supplements boosting intracellular nicotinamide adenine dinucleotide (NAD) levels, thus pre
47 s the major determinant of dependence on the nicotinamide adenine dinucleotide (NAD) metabolic pathwa
49 n variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathwa
55 bosyltransferases such as PARPs that utilize nicotinamide adenine dinucleotide (NAD+) as a cofactor t
57 ed electron transfer (PCET) reaction between nicotinamide adenine dinucleotide (NADH) and a protein-b
58 cleic acids (AAA + NA), tryptophan residues, nicotinamide adenine dinucleotide (NADH) and vitamin A w
60 ine spectral profiles of tryptophan, reduced nicotinamide adenine dinucleotide (NADH), and flavin den
62 decreasing Complex I activity, elevating the nicotinamide adenine dinucleotide (NADH/NAD(+)) ratio an
63 intracellular lactate levels, disrupted the nicotinamide adenine dinucleotide (NADH/NAD(+)) ratio, a
65 olism via endogenous fluorescence of reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H)
68 a common intermediate in the biosynthesis of nicotinamide adenine dinucleotide and its derivatives in
69 skeletal proteins, and loss of intracellular nicotinamide adenine dinucleotide and nicotinamide adeni
70 ctate, with concomitant oxidation of reduced nicotinamide adenine dinucleotide as the final step in t
72 cient oxidative phosphorylation, diminishing nicotinamide adenine dinucleotide concentrations and imp
73 ease in mitochondrial calcium content and in nicotinamide adenine dinucleotide fluorescence following
74 zoles promote neuronal survival by enhancing nicotinamide adenine dinucleotide flux in injured neuron
75 ontaining 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (
76 ins of NLRs are enzymes capable of degrading nicotinamide adenine dinucleotide in its oxidized form (
78 nase 2 was reduced, whereas the NOX2 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase s
79 phatase] oxidase subunit 2) and NOX4 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase s
80 ADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide phosphate (NADP(+) ) f
81 e adenine dinucleotide (NAD(+) and NADH) and nicotinamide adenine dinucleotide phosphate (NADP(+) and
83 chemical analogue exploiting this principle, nicotinamide adenine dinucleotide phosphate (NADPH) and
84 gulate the activity of dFB neurons through a nicotinamide adenine dinucleotide phosphate (NADPH) cofa
85 to support the synthesis and regeneration of nicotinamide adenine dinucleotide phosphate (NADPH) in p
86 is metabolism, reducing power in the form of nicotinamide adenine dinucleotide phosphate (NADPH) is r
87 blast function, activating integrin-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxid
88 8-mediated ROS was generated through reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxid
90 causing hemolytic anemia linked to impaired nicotinamide adenine dinucleotide phosphate (NADPH) prod
92 l and cellular concentration of glutathione, nicotinamide adenine dinucleotide phosphate (NADPH), and
93 ependent protein kinase II), which decreases nicotinamide adenine dinucleotide phosphate hydrogen syn
94 ore, post-R had significantly higher reduced nicotinamide adenine dinucleotide phosphate levels, redu
95 rtate (NMDA) receptor-mediated activation of nicotinamide adenine dinucleotide phosphate oxidase (NOX
96 the STAT5/PI3K/Akt signalling axis and that nicotinamide adenine dinucleotide phosphate oxidase (NOX
100 n peroxide (H(2)O(2)), likely by stimulating nicotinamide adenine dinucleotide phosphate oxidase.
101 downstream effectors such as Rho kinase and nicotinamide adenine dinucleotide phosphate oxidases are
102 reased malondialdehyde, 3-nitrotyrosine, and nicotinamide adenine dinucleotide phosphate oxidases).
103 tive was to investigate the possible role of nicotinamide adenine dinucleotide phosphate reduced form
104 te to cardioprotection by generating reduced nicotinamide adenine dinucleotide phosphate to enhance b
105 of ribose and NADP(+) (the oxidized form of nicotinamide adenine dinucleotide phosphate) complexes o
106 vascular wall include NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase, xa
107 ial susceptibility to NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase-dep
108 ing the cofactors adenosine triphosphate and nicotinamide adenine dinucleotide phosphate, and have be
109 , Shc expression, markers of senescence, and nicotinamide adenine dinucleotide phosphate, reduced for
110 e performed for acetylcholinesterase (AChE), nicotinamide adenine dinucleotide phosphate-diaphorase (
111 enchymal stem/stromal cell therapy decreased nicotinamide adenine dinucleotide phosphate-oxidase 2 an
112 for G6PD enzyme activity, cellular oxidized nicotinamide adenine dinucleotide phosphate/NADPH levels
113 otein adducts together with increased NADPH (nicotinamide adenine dinucleotide phosphateoxidase) acti
114 mic reticulum on electron microscopy, and 3) nicotinamide adenine dinucleotide redox potential and ad
115 tathione/oxidized glutathione (GSH/GSSG) and nicotinamide adenine dinucleotide reduced/oxidized forms
116 ly promoted ROS production by downregulating nicotinamide adenine dinucleotide(+) (NAD(+))/reduced fo
117 d the recently discovered DNA damage-induced nicotinamide adenine dinucleotide(+) depletion to underl
118 thesis of RNA with NADH (the reduced form of nicotinamide adenine dinucleotide) and FAD (flavin adeni
120 ease in the activity of the NAD(+) (oxidized nicotinamide adenine dinucleotide)-dependent deacetylase
121 of extracellular adenosine triphosphate and nicotinamide adenine dinucleotide, both pathways converg
122 e of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) from NA
123 NA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitoch
125 Fe-S center within Complex I (Ndufs1, NADH [nicotinamide adenine dinucleotide] dehydrogenase [ubiqui
126 s we measured the production rate of reduced nicotinamide adenine dinucleotides (NADH) from 91 potent
127 measuring the rates of production of reduced nicotinamide adenine dinucleotides from 91 potential ene
128 cations, including the recently described 5' nicotinamide-adenine dinucleotide (NAD(+)) RNA in bacter
133 ous stage Brugia parasites were incubated in nicotinamide, an agonist of the nematode transient recep
134 a variety showed significant accumulation of nicotinamide and 4-hydroxy-methylglycine in PGPR and PGR
135 in the mother's metabolism of fats, such as nicotinamide and derivatives, rose from virtual absence,
136 er from the cofactor S-adenosylmethionine to nicotinamide and other pyridine-containing compounds.
137 that was expanded ex vivo in the presence of nicotinamide and transplanted after myeloablative condit
139 boflavin, L-asparagine, aspartate, glycerol, nicotinamide, and 3-hydroxy-3-methyglutarate in the leav
140 n A, niacin and riboflavin and milk retinol, nicotinamide, and free riboflavin concentrations in both
142 ketoamide-based 2-(3-phenyl-1H-pyrazol-1-yl)nicotinamides as potent and reversible inhibitors of cal
143 ene moiety, intended to bind the hydrophobic nicotinamide binding pocket via pai-pai stacking interac
144 was enhanced by the sirtuin (SIRT) inhibitor nicotinamide but not by the histone deacetylase inhibito
147 concentrate enzymes and limit distances that nicotinamide cofactors and other metabolites must diffus
151 ycolysis, tricarboxylic acid cycle, OX-PHOS, nicotinamide dinucleotide (NAD(+) ) synthesis, and rever
152 tegrates responses from both redox state and nicotinamide dinucleotide availability to regulate carbo
153 atory complications are prominent, including nicotinamide dinucleotide phosphate oxidase defects in c
155 ays (95% CI, 9 to 14 days) for recipients of nicotinamide-expanded UCB and 21 days (95% CI, 20 to 23
157 ty of TNT was not inhibited by ADP-ribose or nicotinamide, indicating low affinity of TNT for these r
158 MPT) is the rate-limiting enzyme, converting nicotinamide into nicotinamide mononucleotide (NMN).
159 ass spectrometry to the discovery of a novel nicotinamide isoster, the tetrazoloquinoxaline 41, a hig
161 ailed metabolomic analysis revealed elevated nicotinamide metabolism in relapsed LSCs, which activate
162 er, these findings demonstrate that elevated nicotinamide metabolism is both the mechanistic basis fo
163 sferase (NAMPT), the rate-limiting enzyme in nicotinamide metabolism, demonstrated selective eradicat
166 talyzes synthesis of NAADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide
167 We have shown that the NAD(+) precursor, nicotinamide mononucleotide (NMN) can reverse some of th
169 phate and the nicotinamide nucleoside of the nicotinamide mononucleotide (NMN) leaving group are orie
170 by processing NAD(+) and its bio-precursor, nicotinamide mononucleotide (NMN), from tumor microenvir
171 ransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD(+
172 abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the bl
176 levels of the NAD(+) synthesis enzyme Nmnat (nicotinamide mononucleotide adenylyl transferase), but r
177 anges that are associated with a decrease in nicotinamide mononucleotide adenylyltransferase (Nmnat)
178 nicotinamide salvage pathway, constituted by nicotinamide mononucleotide adenylyltransferase (NMNAT)
181 Nicotinamide adenylyl transferase condenses nicotinamide mononucleotide and (tz) ATP to yield N(tz)
183 m of vitamin B3, and its phosphorylated form nicotinamide mononucleotide, have been shown to be poten
186 prominently including the methyltransferase nicotinamide N-methyltransferase (NNMT) and several of t
187 genome mRNA expression profiling identified nicotinamide N-methyltransferase (NNMT) as a downstream
191 isense oligonucleotide knockdown (ASO-KD) of nicotinamide N-methyltransferase (NNMT) in high-fat diet
194 syltransferase (NamPT); 2) the occurrence of nicotinamide N-methyltransferase (NNMT), which diverts n
197 In this study, we examined the ability of nicotinamide (NA) to potentiate the activity of differen
199 ith transcriptome analysis, we discover that nicotinamide (NAM) ameliorated disease-related phenotype
200 oding enzymes for salvage NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while
202 de N-methyltransferase (NNMT), which diverts nicotinamide (Nam) from recycling into NAD, preventing N
206 (NNMT) is a metabolic enzyme that methylates nicotinamide (NAM) using cofactor S-adenosylmethionine (
208 um carbonate (LC; a phosphate binder) and/or nicotinamide (NAM; an inhibitor of active intestinal pho
209 ha phosphate, but the beta phosphate and the nicotinamide nucleoside of the nicotinamide mononucleoti
210 cription of a key NAD(+) biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1).
211 mperatures, may damage the central metabolic nicotinamide nucleotide cofactors [NAD(P)H], generating
216 e age-induced declines of the nicotinate and nicotinamide pathway both in serum and skeletal muscle.
217 reporter, and the perfusion-modifying drugs nicotinamide, pentoxifylline, and hydralazine were used
218 cotinamide adenine dinucleotide (NAD(+)) via nicotinamide phosphoribosyltransferase (Nampt) has emerg
219 thal interaction between PPM1D mutations and nicotinamide phosphoribosyltransferase (NAMPT) inhibitio
225 esized via the NAD(+) salvage pathway, where nicotinamide phosphoribosyltransferase (NAMPT) is the ra
226 we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout
227 roliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels.
230 c knockout of the NAD(+)-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT) reduces l
233 the expression of NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT) via myocy
234 opolysaccharide increase their expression of nicotinamide phosphoribosyltransferase (NAMPT), a key en
236 nonucleotide adenylyltransferase (NMNAT) and nicotinamide phosphoribosyltransferase (NAMPT), mainly r
237 hibitor of the NAD(+) salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT), synergiz
238 g factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate
240 Genetic and pharmacological inhibition of nicotinamide phosphoribosyltransferase (NAMPT), the rate
241 lly, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus lim
243 by deacetylation on lysine 74 and 78 via the nicotinamide phosphoribosyltransferase (NAMPT)/sirtuin 2
244 on of NAD biosynthesis to exclusive usage of nicotinamide phosphoribosyltransferase (NamPT); 2) the o
245 in response to FK866-mediated inhibition of nicotinamide phosphoribosyltransferase and stimulates gl
246 companied by a decrease in expression of the nicotinamide phosphoribosyltransferase enzyme that recyc
248 ely because of transcriptional repression of nicotinamide phosphoribosyltransferase in the NAD(+) sal
250 ects of NR, we generated mice overexpressing nicotinamide phosphoribosyltransferase, a rate-limiting
251 oribosyltransferase enzyme that recycles the nicotinamide precursor, whereas the nicotinamide ribosid
252 centrations has stimulated investigations of nicotinamide riboside (NR) and nicotinamide mononucleoti
253 ide adenine dinucleotide (NAD(+) ) precursor nicotinamide riboside (NR) boosts NAD(+) levels and impr
254 Supplementation with NAD precursors such as nicotinamide riboside (NR) has been shown to enhance mit
258 at supplementation with the NAD(+) precursor nicotinamide riboside (NR) markedly reprograms metabolic
259 human clinical trial to report on effects of nicotinamide riboside (NR) on skeletal muscle mitochondr
260 before and after taking 5 to 9 days of oral nicotinamide riboside (NR), a NAD precursor.RESULTSWe de
261 ge NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while down-regulating other
267 onstrate that azido substitution at 3'-OH of nicotinamide riboside enables enzymatic synthesis of an
269 (+) and inflammation and question the use of nicotinamide riboside in the therapy of inflammatory dis
270 reatment with nicotinamide mononucleotide or nicotinamide riboside increases total NAD(+) content in
271 cles the nicotinamide precursor, whereas the nicotinamide riboside kinase 2 (NMRK2) that phosphorylat
272 sults suggest that elevating NAD levels with nicotinamide riboside may allow animals with cADPR- and
273 otinamide adenine dinucleotide (NAD(+)) with nicotinamide riboside partially blocked neurodegeneratio
274 ide kinase 2 (NMRK2) that phosphorylates the nicotinamide riboside precursor is increased, to a highe
275 In mice subjected to pressure overload, nicotinamide riboside reduced cardiomyocyte death and co
280 n be corrected by the oral administration of nicotinamide riboside, a recently discovered vitamin pre
284 on did not affect the bovine milk content of nicotinamide riboside, whereas UHT processing fully dest
285 F:NADPH product release complex, the reduced nicotinamide ring of the cofactor transiently enters the
286 According to the NADH-bound structure, the nicotinamide ring stacks onto the re-face of the FMN.
288 es for NADase, which selectively cleaves the nicotinamide's glycosidic bond yielding (tz)ADP-ribose.
294 is a key enzyme involved in the recycling of nicotinamide to maintain adequate NAD levels inside the
295 (acitretin, imiquimod, photodynamic therapy, nicotinamide, topical diclofenac, and selenium) and immu
296 NAT1 activity was evaluated in cells after nicotinamide treatment to enhance acetylation or cotrans
297 ycling of NAD(+) consumption products (i.e., nicotinamide) via a salvage pathway in order to maintain
298 Similar results were observed by addition of nicotinamide (vitamin B3), which serves as a methyl grou
299 anisms involved in the circadian response to nicotinamide, we developed a systematic and practical mo
300 cotinic acid adenine dinucleotide and methyl nicotinamide-were elevated in skeletal muscle after NR c