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1 ant metabolites, such as the reduced form of nicotinamide adenine dinucleotide.
2 h wild-type mice, and disrupted the ratio of nicotinamide adenine dinucleotide.
3 P-ribose)polymerase 1 activation, exhausting nicotinamide adenine dinucleotide and adenosine triphosp
4 -cultures to beta-amyloid for >8 h decreased nicotinamide adenine dinucleotide and mitochondrial memb
5 primarily SAM (S-adenosyl methionine), NAD (nicotinamide adenine dinucleotide), and FAD (flavin aden
8 nicotinamide adenine dinucleotide to reduced nicotinamide adenine dinucleotide, as a result of oxidat
9 netics of the signal transducing reaction of nicotinamide adenine dinucleotide at CNTs accounted for
10 functional capillary density: 573+/-13cm/cm; nicotinamide adenine dinucleotide autofluorescence: 56+/
11 functional capillary density: 469+/-22cm/cm; nicotinamide adenine dinucleotide autofluorescence: 61+/
12 ry density: 379+/-20cm/cm;), tissue hypoxia (nicotinamide adenine dinucleotide autofluorescence: 77+/
13 ndicate that another purine nucleotide, beta-nicotinamide adenine dinucleotide (beta-NAD(+)), meets p
15 show that NHDs are NAD(+) (oxidized form of nicotinamide adenine dinucleotide) binding domains that
18 of extracellular adenosine triphosphate and nicotinamide adenine dinucleotide, both pathways converg
19 y to the Shp promoter, which was enhanced by nicotinamide adenine dinucleotide, but not nicotinamide
20 highly sensitive ethanol biosensors based on nicotinamide adenine dinucleotide coenzyme-dependent deh
21 s activated by oxidative stress and consumes nicotinamide adenine dinucleotide, decreasing substrate
22 europathy (LHON) caused by a mutation in the nicotinamide adenine dinucleotide dehydrogenase subunit
23 mastigotes engineered to overexpress reduced nicotinamide adenine dinucleotide dependent nitroreducta
24 ease in the activity of the NAD(+) (oxidized nicotinamide adenine dinucleotide)-dependent deacetylase
25 mutant mouse models to demonstrate that the nicotinamide adenine dinucleotide-dependent (NAD-depende
30 n regulator 2 (Sir2) proteins (sirtuins) are nicotinamide adenine dinucleotide-dependent deacetylases
31 propose a novel mechanism through which the nicotinamide adenine dinucleotide-dependent histone deac
32 otide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contri
33 TDH) from Pseudomonas stutzeri catalyzes the nicotinamide adenine dinucleotide-dependent oxidation of
34 IRT1), the most conserved mammalian oxidized nicotinamide adenine dinucleotide-dependent protein deac
36 lf-ADP ribosylation of PARP1, consumption of nicotinamide adenine dinucleotide(+), diminished adenosi
37 ial mapping, analysis of lactate production, nicotinamide adenine dinucleotide epifluorescence, lacta
38 ellular O(2) and intracellular NADH (reduced nicotinamide adenine dinucleotide), even with lactate de
40 ease in mitochondrial calcium content and in nicotinamide adenine dinucleotide fluorescence following
41 zoles promote neuronal survival by enhancing nicotinamide adenine dinucleotide flux in injured neuron
42 nction, its rediscovery as the key enzyme in nicotinamide adenine dinucleotide generation has conside
43 catenation of FeS and glycerol-dehydrogenase/nicotinamide-adenine-dinucleotide (GlDH-NAD(+)) apoenzym
45 the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.
46 ide, and are present as oxidized and reduced nicotinamide adenine dinucleotides in their unphosphoryl
47 oxidase that helps to regulate intracellular nicotinamide adenine dinucleotide levels in many cell ty
48 mal redox potential, associated with reduced nicotinamide adenine dinucleotide metabolism and altered
49 ion of 2',3'-cyclic phosphate-activated beta-nicotinamide adenine dinucleotide (NAD>p) and ACA>p RNA
50 resembling human fatty liver, lowers hepatic nicotinamide adenine dinucleotide (NAD(+) ) levels drivi
51 enzymes of redox reactions: oxidized/reduced nicotinamide adenine dinucleotide (NAD(+) and NADH) and
52 eously measure oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD(+) and NADH), oxi
54 ruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD(+)) after injury.
56 ypoxia produced PARP1-dependent depletion of nicotinamide adenine dinucleotide (NAD(+)) and inhibitio
57 a common intermediate in the biosynthesis of nicotinamide adenine dinucleotide (NAD(+)) and its deriv
59 ibose units onto substrate proteins by using nicotinamide adenine dinucleotide (NAD(+)) as a cosubstr
60 ld access a Ru-H intermediate using oxidized nicotinamide adenine dinucleotide (NAD(+)) as the H(-) s
61 enylyltransferase, a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD(+)) biosynthesis(
62 anscription feedback loop produces cycles of nicotinamide adenine dinucleotide (NAD(+)) biosynthesis,
64 ver, mammalian mRNAs can also carry a 5' end nicotinamide adenine dinucleotide (NAD(+)) cap that, in
65 al demise is due to severe, neuron-specific, nicotinamide adenine dinucleotide (NAD(+)) depletion.
73 energy stress and oxidative stress response, nicotinamide adenine dinucleotide (NAD(+)) is emerging a
74 nzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism, t
75 by interacting with L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD(+)) metabolism.
76 sfer of ADP-ribose from the oxidized form of nicotinamide adenine dinucleotide (NAD(+)) onto substrat
77 ich transitions to a proton-pumping Fd(red): nicotinamide adenine dinucleotide (NAD(+)) oxidoreductas
80 is critical in maintaining an intracellular nicotinamide adenine dinucleotide (NAD(+)) pool for cont
81 preclinical studies showed the potential of nicotinamide adenine dinucleotide (NAD(+)) precursors to
82 high lactate production, and a high ratio of nicotinamide adenine dinucleotide (NAD(+)) to its reduce
83 a PTM, in which ADP-ribosyltransferases use nicotinamide adenine dinucleotide (NAD(+)) to modify tar
84 ction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD(+)) to that of it
87 y, quantum dots (QDs) modified with cofactor nicotinamide adenine dinucleotide (NAD(+)) were prepared
88 mation of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD(+)), and importan
89 er the ADP-ribose moiety from its substrate, nicotinamide adenine dinucleotide (NAD(+)), to amino aci
90 hibition is dependent on the availability of nicotinamide adenine dinucleotide (NAD(+)), we have hypo
91 resveratrol action is the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent dea
92 rients, which requires the activation of the nicotinamide adenine dinucleotide (NAD(+))-dependent dea
93 4 proteins were first discovered in yeast as nicotinamide adenine dinucleotide (NAD(+))-dependent dea
95 such factor is the sirtuin (SIRT) family of nicotinamide adenine dinucleotide (NAD(+))-dependent dea
96 and the sirtuins as a conserved family of a nicotinamide adenine dinucleotide (NAD(+))-dependent pro
102 that KinA is activated by a decrease in the nicotinamide adenine dinucleotide (NAD(+))/NADH ratio vi
104 ibose (OAADPR) is a metabolite produced from nicotinamide adenine dinucleotide (NAD) as a product of
105 sphate to 1,3-biphosphoglycerate (BPG) using nicotinamide adenine dinucleotide (NAD) as an electron a
106 ns in NMNAT1, which encodes an enzyme in the nicotinamide adenine dinucleotide (NAD) biosynthesis pat
107 of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis.
111 e levels and was up-regulated in response to nicotinamide adenine dinucleotide (NAD) depletion and in
112 ing liver regeneration, the concentration of nicotinamide adenine dinucleotide (NAD) falls, at least
118 be potent supplements boosting intracellular nicotinamide adenine dinucleotide (NAD) levels, thus pre
119 (kcatc) for Rubisco from the C4 grasses with nicotinamide adenine dinucleotide (NAD) phosphate malic
120 SIRT1 and PARP1, that are each consumers of nicotinamide adenine dinucleotide (NAD), a metabolite in
122 Examples include the adduct of glutamate and nicotinamide adenine dinucleotide (NAD), fragments of NA
123 2 family of enzymes or sirtuins are known as nicotinamide adenine dinucleotide (NAD)-dependent deacet
126 Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine
127 a class of enzymes originally identified as nicotinamide adenine dinucleotide (NAD)-dependent protei
131 cations, including the recently described 5' nicotinamide-adenine dinucleotide (NAD(+)) RNA in bacter
132 osphate [ADP]/adenosine monophosphate [AMP], nicotinamide adenine dinucleotide /NAD, nicotinamide ade
133 ly promoted ROS production by downregulating nicotinamide adenine dinucleotide(+) (NAD(+))/reduced fo
134 ltammetric determination of cysteamine (CA), nicotinamide adenine dinucleotide (NADH) and folic acid
135 s and produce in situ chemical species (beta-nicotinamide adenine dinucleotide (NADH) and H2O2) actin
136 sk electrode for simultaneous measurement of nicotinamide adenine dinucleotide (NADH) and hydrogen pe
137 1 mediates reduction of the diiron center by nicotinamide adenine dinucleotide (NADH) and initiates O
138 to pyruvate to form l-lactate, using reduced nicotinamide adenine dinucleotide (NADH) as the cofactor
139 le electrochemical sensing platform for beta-nicotinamide adenine dinucleotide (NADH) based on uncapp
141 inetic assay detecting the intrinsic reduced nicotinamide adenine dinucleotide (NADH) fluorescence an
142 ivo and noninvasively the changes in reduced nicotinamide adenine dinucleotide (NADH) fluorescence of
143 rts was associated with a marked decrease in nicotinamide adenine dinucleotide (NADH) fluorescence, l
144 de adenine dinucleotide phosphate (NADPH) to nicotinamide adenine dinucleotide (NADH) have been made
145 e new sensor were tested by the oxidation of nicotinamide adenine dinucleotide (NADH) in a 0.1 M Robi
146 mediators for the oxidation of reduced beta-nicotinamide adenine dinucleotide (NADH) in two polymeri
149 l alcohol sensing, whereby the coenzyme beta-Nicotinamide adenine dinucleotide (NADH) is employed as
150 uction in dye-sensitized solar cells and for nicotinamide adenine dinucleotide (NADH) oxidation in de
151 ith the intracellular application of reduced nicotinamide adenine dinucleotide (NADH), an effect that
152 ine spectral profiles of tryptophan, reduced nicotinamide adenine dinucleotide (NADH), and flavin den
153 to analyze hydrogen peroxide (H2O2) and beta-nicotinamide adenine dinucleotide (NADH), obtaining subs
154 se that is stimulated by the reduced form of nicotinamide adenine dinucleotide (NADH), suggesting a s
156 ew electrode material for the development of nicotinamide adenine dinucleotide (NADH)-based biosensor
160 We assessed the reduced/oxidized ratio of nicotinamide adenine dinucleotide (NADH/NAD(+) ratio) an
161 active oxygen species (ROS) by the phagocyte nicotinamide adenine dinucleotide (NADPH) oxidase in pat
162 e R204Q variant results in the uncoupling of nicotinamide adenine dinucleotide oxidation from uric ac
165 cleus and that this source of ROS is reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) ox
166 translocation of the cytosolic components of nicotinamide adenine dinucleotide phosphate (NAD(P)H)-ox
167 e adenine dinucleotide (NAD(+) and NADH) and nicotinamide adenine dinucleotide phosphate (NADP(+) and
168 (+) and NADH), oxidized and reduced forms of nicotinamide adenine dinucleotide phosphate (NADP(+) and
169 glucose-6-phosphate dehydrogenase (G6PD) and nicotinamide adenine dinucleotide phosphate (NADP(+)); t
171 oduction of reactive oxygen species (ROS) by nicotinamide adenine dinucleotide phosphate (NADPH) 2 (N
172 dehyde as substrates and the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) as c
173 to support the synthesis and regeneration of nicotinamide adenine dinucleotide phosphate (NADPH) in p
175 each strain when cellular demand for reduced nicotinamide adenine dinucleotide phosphate (NADPH) is g
177 sing intravital microscopy with mice lacking nicotinamide adenine dinucleotide phosphate (NADPH) oxid
178 ation of p47(phox) (an organizer subunit for nicotinamide adenine dinucleotide phosphate (NADPH) oxid
179 ng protein 9 (CARD9), but was independent of nicotinamide adenine dinucleotide phosphate (NADPH) oxid
180 because of defective activation of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxid
181 s in the genes that encode components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxid
183 blast function, activating integrin-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxid
184 Instead, ROS generation was mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxid
187 logic stretch rapidly activates reduced-form nicotinamide adenine dinucleotide phosphate (NADPH) oxid
189 However, gp91(phox) and p22(phox) reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxid
190 8-mediated ROS was generated through reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxid
192 neutrophils exhibited reduced (hydrogenated) nicotinamide adenine dinucleotide phosphate (NADPH) oxid
193 this study, we show that antibiotics rescue nicotinamide adenine dinucleotide phosphate (NADPH) oxid
194 ure to LPS led to up-regulated expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxid
195 causing hemolytic anemia linked to impaired nicotinamide adenine dinucleotide phosphate (NADPH) prod
196 s, G6PD is upregulated and generates reduced nicotinamide adenine dinucleotide phosphate (NADPH) that
197 cofactor specificity of oxidoreductases from nicotinamide adenine dinucleotide phosphate (NADPH) to n
199 the enzyme with acyl-coenzyme A and reduced nicotinamide adenine dinucleotide phosphate (NADPH), a p
200 operoxidase (LPO) and myeloperoxidase (MPO), nicotinamide adenine dinucleotide phosphate (NADPH)-depe
201 vealed age-related changes in the density of nicotinamide adenine dinucleotide phosphate (NADPH)-diap
202 , which exhibited decreased steatohepatitis, nicotinamide adenine dinucleotide phosphate (NADPH)-oxid
203 y immunodeficiency caused by a defect in the nicotinamide adenine dinucleotide phosphate (NADPH)-oxid
204 ministered to block superoxide production by nicotinamide adenine dinucleotide phosphate (NADPH).
205 icotinamide adenine dinucleotide phosphate / nicotinamide adenine dinucleotide phosphate , flavin ade
206 MP], nicotinamide adenine dinucleotide /NAD, nicotinamide adenine dinucleotide phosphate / nicotinami
207 rtas of wild-type mice or mice deficient for nicotinamide adenine dinucleotide phosphate [NAD(P)H] ox
209 ependent protein kinase II), which decreases nicotinamide adenine dinucleotide phosphate hydrogen syn
211 his, as well as the observation that reduced nicotinamide adenine dinucleotide phosphate oxidase (NAD
212 ivity for macrophages and myofibroblasts and nicotinamide adenine dinucleotide phosphate oxidase (NOX
217 uced blood pressure, whereas the transfer of nicotinamide adenine dinucleotide phosphate oxidase 2-de
219 nulomatous disease (CGD) is due to defective nicotinamide adenine dinucleotide phosphate oxidase acti
220 the signal involves plasma membrane reduced nicotinamide adenine dinucleotide phosphate oxidase acti
221 p47(phox) subunit beyond and independent of nicotinamide adenine dinucleotide phosphate oxidase acti
222 at adiponectin directly decreases myocardial nicotinamide adenine dinucleotide phosphate oxidase acti
223 rated that adiponectin suppresses myocardial nicotinamide adenine dinucleotide phosphate oxidase acti
224 neuroinflammation by selectively inhibiting nicotinamide adenine dinucleotide phosphate oxidase and
225 the generation of reactive oxygen species by nicotinamide adenine dinucleotide phosphate oxidase and
226 euron death through activation of microglial nicotinamide adenine dinucleotide phosphate oxidase and
227 blocked agonist-initiated association of the nicotinamide adenine dinucleotide phosphate oxidase comp
228 airment through neurohormonal activation of (nicotinamide adenine dinucleotide phosphate oxidase depe
229 oxidative stress, including up-regulation of nicotinamide adenine dinucleotide phosphate oxidase in a
230 ing the efficacy of an ultra-low dose of the nicotinamide adenine dinucleotide phosphate oxidase inhi
231 ), TEMPOL (a general antioxidant), apocynin (nicotinamide adenine dinucleotide phosphate oxidase inhi
233 either poly(ADP-ribose) polymerase or of the nicotinamide adenine dinucleotide phosphate oxidase prev
234 xpression in P47 and Rac-1 expression of two nicotinamide adenine dinucleotide phosphate oxidase subu
236 ed baroreflex sensitivity is associated with nicotinamide adenine dinucleotide phosphate oxidase subu
238 own experimentally to activate transmembrane nicotinamide adenine dinucleotide phosphate oxidase type
239 th P67 dominant negative mice to inhibit the nicotinamide adenine dinucleotide phosphate oxidase were
243 show that the oxidative burst, catalyzed by nicotinamide adenine dinucleotide phosphate oxidase, can
244 to beta-amyloid peptides activates the glial nicotinamide adenine dinucleotide phosphate oxidase, fol
245 cleotide phosphate oxidase 4 (Nox4), a major nicotinamide adenine dinucleotide phosphate oxidase, med
246 drial electron transport chain reactions and nicotinamide adenine dinucleotide phosphate oxidase, or
247 uncoupled endothelial nitric oxide synthase, nicotinamide adenine dinucleotide phosphate oxidase, xan
250 tion by restoring renal blood flow, reducing nicotinamide adenine dinucleotide phosphate oxidase-deri
251 oding adiponectin) led to reduced myocardial nicotinamide adenine dinucleotide phosphate oxidase-deri
253 regulated by growth factors and Nox4 reduced nicotinamide adenine dinucleotide phosphate oxidase.
254 oxidative stress generated by the astrocytic nicotinamide adenine dinucleotide phosphate oxidase.
255 s attributable to constitutive activation of nicotinamide adenine dinucleotide phosphate oxidases (NO
256 activation, implicating a crosstalk between nicotinamide adenine dinucleotide phosphate oxidases and
257 downstream effectors such as Rho kinase and nicotinamide adenine dinucleotide phosphate oxidases are
258 Dual oxidases (DUOX) are conserved reduced nicotinamide adenine dinucleotide phosphate oxidases tha
259 omic DNA was extracted and genotyped for the nicotinamide adenine dinucleotide phosphate p22 phagocyt
260 tive was to investigate the possible role of nicotinamide adenine dinucleotide phosphate reduced form
261 nship between two membrane transporters, the Nicotinamide adenine dinucleotide phosphate reduced form
262 e hypothesized that AGEs induce TACE through nicotinamide adenine dinucleotide phosphate reduced oxid
264 enzyme that mediates electron transfer from nicotinamide adenine dinucleotide phosphate to molecular
265 NADPH/NADP(+) (the reduced form of NADP(+)/nicotinamide adenine dinucleotide phosphate) homeostasis
266 vascular wall include NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase, xa
267 ial susceptibility to NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase-dep
268 ing the cofactors adenosine triphosphate and nicotinamide adenine dinucleotide phosphate, and have be
269 derivatives in complex with PfIspC, reduced nicotinamide adenine dinucleotide phosphate, and Mg(2+)
270 ion, depleting and oxidizing glutathione and nicotinamide adenine dinucleotide phosphate, and signifi
271 osynthetic electron transport in the form of nicotinamide adenine dinucleotide phosphate, reduced are
272 nockout, PBL13 is able to associate with the nicotinamide adenine dinucleotide phosphate, reduced oxi
273 forms of nicotinamide adenine nucleotide and nicotinamide adenine dinucleotide phosphate, respectivel
276 e performed for acetylcholinesterase (AChE), nicotinamide adenine dinucleotide phosphate-diaphorase (
278 enchymal stem/stromal cell therapy decreased nicotinamide adenine dinucleotide phosphate-oxidase 2 an
281 for G6PD enzyme activity, cellular oxidized nicotinamide adenine dinucleotide phosphate/NADPH levels
282 terleukin-10, protein expressions of reduced nicotinamide-adenine dinucleotide phosphate:quinone oxid
283 olism via endogenous fluorescence of reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H)
285 mic reticulum on electron microscopy, and 3) nicotinamide adenine dinucleotide redox potential and ad
287 The brain depends on redox electrons from nicotinamide adenine dinucleotide (reduced form; NADH) t
288 ubunits of the RNA polymerase, and thylakoid nicotinamide adenine dinucleotide (reduced) and cytochro
289 hain reaction) and oxidative phosphorylation nicotinamide adenine dinucleotide (reduced) dehydrogenas
290 inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and ace
291 ence of C-SWCNT, the oxidation of NADH (beta-nicotinamide adenine dinucleotide, reduced form) and DTT
292 acetate production to the formation of NADH (nicotinamide adenine dinucleotide, reduced form) that is
293 esults in the concomitant oxidation of NADH (nicotinamide adenine dinucleotide, reduced form) to NAD(
295 ng, and hematoxylin-eosin (10 specimens) and nicotinamide adenine dinucleotide (six specimens) staini
297 etabolic dependencies (fatty acid oxidation, nicotinamide adenine dinucleotide synthesis, glutamine b
298 witch, we demonstrated that depletion of the nicotinamide adenine dinucleotide synthetase (NadE) rapi
299 ms-ethanol by reducing the ratio of oxidized nicotinamide adenine dinucleotide to reduced nicotinamid
300 n catalysed by these enzymes is energized by nicotinamide adenine dinucleotide, which activates ubiqu
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