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1 rmacokinetics to those of nicotinic acid and nicotinamide.
2 athway capable of resynthesizing NAD(+) from nicotinamide.
3 h postintervention period, and the safety of nicotinamide.
4 hat can be normalized by the anti-aging drug nicotinamide.
5 f 2,3,4-trihydroxy-5-methylacetophenone (1), nicotinamide (2), and uracil (3) from palmyra palm syrup
6 that 8 extracellular compounds (lactic acid, nicotinamide, 5-oxoproline, xanthine, hypoxanthine, gluc
7 ment in vivo with the NAD(+) repleting agent nicotinamide, a form of vitamin B3, prevented thymus atr
8 namide N-methyltransferase (Nnmt) methylates nicotinamide, a form of vitamin B3, to produce N(1)-meth
10 ine dinucleotide(+) (NAD(+))/reduced form of nicotinamide adenine dinucleotid (NADH) ratio and the NA
11 resembling human fatty liver, lowers hepatic nicotinamide adenine dinucleotide (NAD(+) ) levels drivi
12 enzymes of redox reactions: oxidized/reduced nicotinamide adenine dinucleotide (NAD(+) and NADH) and
13 eously measure oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD(+) and NADH), oxi
14 ruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD(+)) after injury.
15 a common intermediate in the biosynthesis of nicotinamide adenine dinucleotide (NAD(+)) and its deriv
17 ld access a Ru-H intermediate using oxidized nicotinamide adenine dinucleotide (NAD(+)) as the H(-) s
18 ver, mammalian mRNAs can also carry a 5' end nicotinamide adenine dinucleotide (NAD(+)) cap that, in
19 al demise is due to severe, neuron-specific, nicotinamide adenine dinucleotide (NAD(+)) depletion.
23 energy stress and oxidative stress response, nicotinamide adenine dinucleotide (NAD(+)) is emerging a
24 sfer of ADP-ribose from the oxidized form of nicotinamide adenine dinucleotide (NAD(+)) onto substrat
27 preclinical studies showed the potential of nicotinamide adenine dinucleotide (NAD(+)) precursors to
28 a PTM, in which ADP-ribosyltransferases use nicotinamide adenine dinucleotide (NAD(+)) to modify tar
29 ction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD(+)) to that of it
31 y, quantum dots (QDs) modified with cofactor nicotinamide adenine dinucleotide (NAD(+)) were prepared
32 such factor is the sirtuin (SIRT) family of nicotinamide adenine dinucleotide (NAD(+))-dependent dea
33 resveratrol action is the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent dea
34 rients, which requires the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent dea
38 of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis.
41 ing liver regeneration, the concentration of nicotinamide adenine dinucleotide (NAD) falls, at least
46 be potent supplements boosting intracellular nicotinamide adenine dinucleotide (NAD) levels, thus pre
47 (kcatc) for Rubisco from the C4 grasses with nicotinamide adenine dinucleotide (NAD) phosphate malic
48 SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite in
49 Examples include the adduct of glutamate and nicotinamide adenine dinucleotide (NAD), fragments of NA
52 a class of enzymes originally identified as nicotinamide adenine dinucleotide (NAD)-dependent protei
53 s and produce in situ chemical species (beta-nicotinamide adenine dinucleotide (NADH) and H2O2) actin
54 to pyruvate to form l-lactate, using reduced nicotinamide adenine dinucleotide (NADH) as the cofactor
58 ine spectral profiles of tryptophan, reduced nicotinamide adenine dinucleotide (NADH), and flavin den
60 ew electrode material for the development of nicotinamide adenine dinucleotide (NADH)-based biosensor
63 We assessed the reduced/oxidized ratio of nicotinamide adenine dinucleotide (NADH/NAD(+) ratio) an
64 active oxygen species (ROS) by the phagocyte nicotinamide adenine dinucleotide (NADPH) oxidase in pat
65 olism via endogenous fluorescence of reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H)
67 ubunits of the RNA polymerase, and thylakoid nicotinamide adenine dinucleotide (reduced) and cytochro
68 osphate [ADP]/adenosine monophosphate [AMP], nicotinamide adenine dinucleotide /NAD, nicotinamide ade
72 ease in mitochondrial calcium content and in nicotinamide adenine dinucleotide fluorescence following
73 zoles promote neuronal survival by enhancing nicotinamide adenine dinucleotide flux in injured neuron
75 mal redox potential, associated with reduced nicotinamide adenine dinucleotide metabolism and altered
76 (+) and NADH), oxidized and reduced forms of nicotinamide adenine dinucleotide phosphate (NADP(+) and
77 e adenine dinucleotide (NAD(+) and NADH) and nicotinamide adenine dinucleotide phosphate (NADP(+) and
79 dehyde as substrates and the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) as c
80 to support the synthesis and regeneration of nicotinamide adenine dinucleotide phosphate (NADPH) in p
82 neutrophils exhibited reduced (hydrogenated) nicotinamide adenine dinucleotide phosphate (NADPH) oxid
83 this study, we show that antibiotics rescue nicotinamide adenine dinucleotide phosphate (NADPH) oxid
84 ure to LPS led to up-regulated expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxid
86 sing intravital microscopy with mice lacking nicotinamide adenine dinucleotide phosphate (NADPH) oxid
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 icotinamide adenine dinucleotide phosphate / nicotinamide adenine dinucleotide phosphate , flavin ade
93 MP], nicotinamide adenine dinucleotide /NAD, nicotinamide adenine dinucleotide phosphate / nicotinami
94 ependent protein kinase II), which decreases nicotinamide adenine dinucleotide phosphate hydrogen syn
97 uced blood pressure, whereas the transfer of nicotinamide adenine dinucleotide phosphate oxidase 2-de
98 at adiponectin directly decreases myocardial nicotinamide adenine dinucleotide phosphate oxidase acti
99 rated that adiponectin suppresses myocardial nicotinamide adenine dinucleotide phosphate oxidase acti
100 nulomatous disease (CGD) is due to defective nicotinamide adenine dinucleotide phosphate oxidase acti
101 airment through neurohormonal activation of (nicotinamide adenine dinucleotide phosphate oxidase depe
102 ing the efficacy of an ultra-low dose of the nicotinamide adenine dinucleotide phosphate oxidase inhi
104 ed baroreflex sensitivity is associated with nicotinamide adenine dinucleotide phosphate oxidase subu
106 own experimentally to activate transmembrane nicotinamide adenine dinucleotide phosphate oxidase type
109 show that the oxidative burst, catalyzed by nicotinamide adenine dinucleotide phosphate oxidase, can
110 oding adiponectin) led to reduced myocardial nicotinamide adenine dinucleotide phosphate oxidase-deri
112 downstream effectors such as Rho kinase and nicotinamide adenine dinucleotide phosphate oxidases are
113 nship between two membrane transporters, the Nicotinamide adenine dinucleotide phosphate reduced form
114 tive was to investigate the possible role of nicotinamide adenine dinucleotide phosphate reduced form
115 NADPH/NADP(+) (the reduced form of NADP(+)/nicotinamide adenine dinucleotide phosphate) homeostasis
116 vascular wall include NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase, xa
117 ial susceptibility to NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase-dep
118 ing the cofactors adenosine triphosphate and nicotinamide adenine dinucleotide phosphate, and have be
119 ion, depleting and oxidizing glutathione and nicotinamide adenine dinucleotide phosphate, and signifi
120 nockout, PBL13 is able to associate with the nicotinamide adenine dinucleotide phosphate, reduced oxi
121 forms of nicotinamide adenine nucleotide and nicotinamide adenine dinucleotide phosphate, respectivel
124 e performed for acetylcholinesterase (AChE), nicotinamide adenine dinucleotide phosphate-diaphorase (
125 enchymal stem/stromal cell therapy decreased nicotinamide adenine dinucleotide phosphate-oxidase 2 an
128 for G6PD enzyme activity, cellular oxidized nicotinamide adenine dinucleotide phosphate/NADPH levels
129 mic reticulum on electron microscopy, and 3) nicotinamide adenine dinucleotide redox potential and ad
130 ly promoted ROS production by downregulating nicotinamide adenine dinucleotide(+) (NAD(+))/reduced fo
131 show that NHDs are NAD(+) (oxidized form of nicotinamide adenine dinucleotide) binding domains that
132 primarily SAM (S-adenosyl methionine), NAD (nicotinamide adenine dinucleotide), and FAD (flavin aden
133 ease in the activity of the NAD(+) (oxidized nicotinamide adenine dinucleotide)-dependent deacetylase
134 of extracellular adenosine triphosphate and nicotinamide adenine dinucleotide, both pathways converg
135 y to the Shp promoter, which was enhanced by nicotinamide adenine dinucleotide, but not nicotinamide
136 inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and ace
137 n catalysed by these enzymes is energized by nicotinamide adenine dinucleotide, which activates ubiqu
139 otide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contri
141 ates that transgenic expression of bacterial nicotinamide adenine mononucleotide (NMN) in zebrafish a
142 n, with NADH and NADPH (the reduced forms of nicotinamide adenine nucleotide and nicotinamide adenine
143 cations, including the recently described 5' nicotinamide-adenine dinucleotide (NAD(+)) RNA in bacter
144 catenation of FeS and glycerol-dehydrogenase/nicotinamide-adenine-dinucleotide (GlDH-NAD(+)) apoenzym
150 in the mother's metabolism of fats, such as nicotinamide and derivatives, rose from virtual absence,
151 ynurenic acid, anthranilic acid, tryptophan, nicotinamide and N1-methylnicotinamide were measured in
154 udy linking maternal serum concentrations of nicotinamide and related metabolites to the risk of atop
155 a toxin subunit A (CTA), which hydrolyze the nicotinamide and transfer (tz)ADP-ribose to an arginine
157 acids (taurocholate and glycodeoxycholate), nicotinamide, and adenosine-5-phosphate were significant
158 hat the effects of the pan-sirtuin inhibitor nicotinamide are primarily mediated by SIRT1 inhibition.
159 Because all of the above enzymes generate nicotinamide as a byproduct, mammalian cells have evolve
160 ketoamide-based 2-(3-phenyl-1H-pyrazol-1-yl)nicotinamides as potent and reversible inhibitors of cal
161 ed by treatment with NAD(+) or its precursor nicotinamide because of restoration of physiological NAD
162 docking of inhibitors to the NNMT substrate (nicotinamide)-binding site produced a robust correlation
164 miscuity that uses the photoexcited state of nicotinamide co-factors (molecules that assist enzyme-me
165 echanisms of enzymatic hydride transfer with nicotinamide coenzyme biomimetics (NCBs) is critical to
167 ive, but they rely on unstable and expensive nicotinamide coenzymes that have prevented their widespr
168 (PGMs) can give a dose-dependent response to nicotinamide coenzymes, such as the reduced form of nico
170 at were based on a 5-aminonaphthalen-1-yloxy nicotinamide core structure, 5-((3-amidobenzyl)oxy)nicot
171 Under irradiation with visible light, the nicotinamide-dependent enzyme known as ketoreductase can
173 oxidised (NAD+ and NADP+) and reduced (NADH) nicotinamide dinucleotides, which therapy decreased gene
174 Similar differences were found between the nicotinamide group and the placebo group with respect to
175 5% confidence interval [CI], 4 to 38) in the nicotinamide group than in the placebo group (P=0.02).
176 er of actinic keratoses was 11% lower in the nicotinamide group than in the placebo group at 3 months
178 ass spectrometry to the discovery of a novel nicotinamide isoster, the tetrazoloquinoxaline 41, a hig
179 metabolism of lipids, glucose, fatty acids, nicotinamide, lysosome, insulin signaling and type 1 dia
180 AD precursor niacinamide (NAM, also known as nicotinamide), marked fat accumulation, and failure to r
181 or vitamin B3 derivatives, such as niacin or nicotinamide, may reduce dietary phosphate absorption an
182 pathways including striking accumulations of nicotinamide mononucleotide (NMN) and nicotinamide ribos
183 We have shown that the NAD(+) precursor, nicotinamide mononucleotide (NMN) can reverse some of th
184 phate and the nicotinamide nucleoside of the nicotinamide mononucleotide (NMN) leaving group are orie
185 plementation with NAD(+) precursors, such as nicotinamide mononucleotide (NMN) or nicotinamide ribosi
189 we show that NAD(+), the metabolite of WldS/nicotinamide mononucleotide adenylyltransferase enzymati
190 Nicotinamide adenylyl transferase condenses nicotinamide mononucleotide and (tz) ATP to yield N(tz)
191 neous quantitation of nicotinamide riboside, nicotinamide mononucleotide and NAD in milk by means of
192 Supplementation with the NAD(+) precursors nicotinamide mononucleotide and nicotinamide riboside al
194 -IA, can dephosphorylate the mononucleotides nicotinamide mononucleotide and nicotinic acid mononucle
195 require high (millimolar) concentrations of nicotinamide mononucleotide or NAMN for efficient cataly
197 m of vitamin B3, and its phosphorylated form nicotinamide mononucleotide, have been shown to be poten
199 mited gene expression changes, but had lower nicotinamide N-methyl transferase (NNMT) levels and were
200 genome mRNA expression profiling identified nicotinamide N-methyltransferase (NNMT) as a downstream
203 to the discovery of a covalent inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme impli
205 rmidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyami
206 e--a 28 d HFD-induced model of obesity and a nicotinamide (NA)-streptozotocin (STZ)-HFD-induced model
207 D-induced obesity and insulin resistance and nicotinamide (NA)-streptozotocin (STZ)-HFD-induced type
208 ith transcriptome analysis, we discover that nicotinamide (NAM) ameliorated disease-related phenotype
211 ces two novel metabolites by phosphorylating nicotinamide/nicotinic acid adenine dinucleotide at the
212 ha phosphate, but the beta phosphate and the nicotinamide nucleoside of the nicotinamide mononucleoti
216 adenine nucleotide translocator 1 (ANT1) and nicotinamide nucleotide transhydrogenase (NNT)], we sele
218 On the contrary, most of the purine and nicotinamide nucleotides, acetoacetyl-CoA, H2O2, reduced
219 namide core structure, 5-((3-amidobenzyl)oxy)nicotinamides offered excellent activity against SIRT2 a
221 vage pathway genes pncA and pncB, for use of nicotinamide or nicotinic acid, respectively, for NAD sy
223 omas (20% [95% CI, -6 to 39] lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (
224 reporter, and the perfusion-modifying drugs nicotinamide, pentoxifylline, and hydralazine were used
225 dated salvage pathway despite no increase in nicotinamide phosphoribosyl transferase or in the NR tra
226 (cKO) and cardiac-specific overexpression of nicotinamide phosphoribosyltransferase (cNAMPT) as examp
228 cotinamide adenine dinucleotide (NAD(+)) via nicotinamide phosphoribosyltransferase (Nampt) has emerg
229 ensitizing to NAD+ depletion via concomitant nicotinamide phosphoribosyltransferase (NAMPT) inhibitio
233 roliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels.
236 iosynthesis inhibitors, specifically against nicotinamide phosphoribosyltransferase (NAMPT), as precl
237 anied with significant decrease of SIRT1 and nicotinamide phosphoribosyltransferase (NAMPT), SIRT1 ac
239 in response to FK866-mediated inhibition of nicotinamide phosphoribosyltransferase and stimulates gl
240 companied by a decrease in expression of the nicotinamide phosphoribosyltransferase enzyme that recyc
242 ely because of transcriptional repression of nicotinamide phosphoribosyltransferase in the NAD(+) sal
245 ects of NR, we generated mice overexpressing nicotinamide phosphoribosyltransferase, a rate-limiting
246 of the rate-limiting enzyme in this pathway, nicotinamide phosphoribosyltransferase, increases total
247 iosynthesis only in muscle by overexpressing nicotinamide phosphoribosyltransferase, the rate-limitin
248 as supplementation with the NAMPT substrate, nicotinamide, potentiated a subthreshold dose of P7C3-A2
249 oribosyltransferase enzyme that recycles the nicotinamide precursor, whereas the nicotinamide ribosid
253 crease RPE differentiation; combination with nicotinamide resulted in conversion of over one-half of
256 -1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derange
257 Nicotinamide and nicotinic acid as well as nicotinamide riboside (NR) and nicotinic acid riboside (
259 ons of nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) in the amidated salvage pathw
261 Additionally, deletion of SSY5 increases nicotinamide riboside (NR) levels and phosphate-responsi
262 the rate of liver regeneration, we supplied nicotinamide riboside (NR), an NAD precursor, in the dri
263 such as nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), protects against metabolic d
264 ) precursors nicotinamide mononucleotide and nicotinamide riboside also increases NAD(+) levels in as
265 c precursors nicotinamide mononucleotide and nicotinamide riboside are reported to confer resistance
268 cles the nicotinamide precursor, whereas the nicotinamide riboside kinase 2 (NMRK2) that phosphorylat
269 ide kinase 2 (NMRK2) that phosphorylates the nicotinamide riboside precursor is increased, to a highe
273 ion on the development of steatosis in mice, nicotinamide riboside, a precursor of NAD(+) biosynthesi
274 methotrexate, supplementation of a diet with nicotinamide riboside, an NAD precursor, replenished hep
275 rst time on the simultaneous quantitation of nicotinamide riboside, nicotinamide mononucleotide and N
276 assess the effects of the sirtuin activator, nicotinamide riboside, on NLRP3 inflammasome activation.
279 on did not affect the bovine milk content of nicotinamide riboside, whereas UHT processing fully dest
282 F:NADPH product release complex, the reduced nicotinamide ring of the cofactor transiently enters the
285 es for NADase, which selectively cleaves the nicotinamide's glycosidic bond yielding (tz)ADP-ribose.
286 which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associ
287 AxD induced by pharmacological inhibition of nicotinamide salvage, both NAD(+) and NR prevent neurona
288 (ADPR), cyclic ADPR, and nicotinamide, with nicotinamide serving as a feedback inhibitor of the enzy
290 tested the ability of NADH, ADP-ribose, and nicotinamide to inhibit these NAD(+)-dependent deacylase
291 is a key enzyme involved in the recycling of nicotinamide to maintain adequate NAD levels inside the
296 Oral administration of the NAD(+) precursor nicotinamide (vitamin B3), and/or gene therapy (driving
300 (+) into ADP-ribose (ADPR), cyclic ADPR, and nicotinamide, with nicotinamide serving as a feedback in
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