ライフサイエンスコーパス: NAD

1 levels of nicotinamide adenine dinucleotide (NAD(+)).

2 corresponding processes with the nonemissive NAD(+).

3 , and subsequent Sarm-dependent depletion of NAD(+).

4 cRK-I.8 enhances the Arabidopsis response to NAD(+).

5 th active disease (AD) or nonactive disease (NAD).

6 e patients had reduced levels of circulating NAD.

7 oute of electron transfer from ferredoxin to NAD.

8 1) is an alternative to LDH as a supplier of NAD.

9 also decreases the nucleolar association of NADs.

10 n the apo-form (refined to 1.35 A), bound to NAD(+) (1.45 A), and bound to NADH (1.79 A).

11 tion of the three-coordinate imido ((Ar)L)Fe(NAd) (5) with chlorotriphenylmethane afforded ((Ar)L)FeC

12 lorotriphenylmethane afforded ((Ar)L)FeCl((*)NAd) (6) with concomitant expulsion of Ph3C(C6H5)CPh2.

13 levels of nicotinamide adenine dinucleotide (NAD(+), a key molecule in energy and redox metabolism) d

14 supports increased glycolysis by generating NAD(+), a substrate for GAPDH-mediated glycolytic reacti

15 on creates the need for a constant supply of NAD, a co-factor in glycolysis.

16 hich is 3.5-fold longer than that of the INH-NAD adduct formed by the tuberculosis drug, isoniazid.

17 omplex lowers the lysine pKa and engages the NAD(+) alpha phosphate, but the beta phosphate and the n

18 cs, and biochemical utility of a fluorescent NAD(+) analogue based on an isothiazolo[4,3-d]pyrimidine

19 a profound increase in the hydrolysis of ATP/NAD and AMP, resulting primarily from the upregulation o

20 tion of NAD synthesis caused a deficiency of NAD and congenital malformations in humans and mice.

21 o required for the nucleolar localization of NADs and Ki-67 during interphase.

22 sm for how the "deNADding" reaction produces NAD(+) and 5' phosphate RNA.

23 Ligases react with ATP or NAD(+) and a divalent cation cofactor to form a covalent

24 found that in the absence of HSF1, levels of NAD(+) and ATP are not efficiently sustained in hepatic

25 Mechanistically, the defect in NAD(+) and ATP synthesis linked to a loss of NAD(+)-depe

26 ate-based inhibitor and the enzyme cofactors NAD(+) and inorganic phosphate.

27 d/reduced nicotinamide adenine dinucleotide (NAD(+) and NADH) and nicotinamide adenine dinucleotide p

28 +) to NR prompted us to probe the effects of NAD(+) and NR in protection against excitotoxicity.

29 cal inhibition of nicotinamide salvage, both NAD(+) and NR prevent neuronal death and AxD in a manner

30 Dtx3L heterodimerization with Parp9 enables NAD(+) and poly(ADP-ribose) regulation of E3 activity.

31 amounts of ROS in the presence of Mg(2+) and NAD(+) and the absence of exogenous substrates upon inne

32 titive toward both the peptide substrate and NAD(+), and the crystal structure of a 1,2,4-oxadiazole

33 lic enzyme by increases in matrix [Mg(2+)], [NAD(+)], and [ADP].

34 (S = 5/2), three-coordinate imidos ((Ar)L)Fe(NAd) and ((Ar)L)Fe(NMes), respectively, as determined by

35 hosphate, fructose 6-phosphate and oxidised (NAD+ and NADP+) and reduced (NADH) nicotinamide dinucleo

36 We show that the affinity to NAD+ and UDP-containing factors during initiation is muc

37 on both MDH1 and LDH to replenish cytosolic NAD, and that therapies designed at targeting glycolysis

38 specific loci (nucleolar-associated domains [NADs]) and proteins to the nucleolus during interphase.

39 Here we show that, apart from NAD+, another adenosine-containing cofactor FAD and high

40 Our findings establish NAD(+) as an alternative mammalian RNA cap and DXO as a

41 the reaction, HDH utilises two molecules of NAD(+) as the hydride acceptor.

42 P-ribose) polymerase, resulting in extensive NAD(+)/ATP depletion.

43 NAD availability is limiting during liver regeneration,

44 To test whether NAD availability restricts the rate of liver regeneratio

45 compromised in mutant cells due to decreased NAD(+) availability.

46 family TIGR03971 contain an insertion at the NAD binding site.

47 ise structural rearrangements that allow for NAD(+) binding for the first time.

48 Mutation of the NAD(+) binding site in Parp9 increases the DNA repair ac

49 that inhibitory residues tethered within the NAD(+)-binding site by an intramolecular disulfide in th

50 k the nadA and nadB genes needed for de novo NAD biosynthesis, remarkably, they have one de novo path

51 sphoribosyltransferase gene, responsible for NAD biosynthesis, was among the top downregulated transc

52 anisms prioritize their use of pyridines for NAD biosynthesis.

53 In conclusion, NAPRT-dependent NAD(+) biosynthesis contributes to cell metabolism and t

54 This mechanism for NAD(+) biosynthesis creates novel possibilities for mani

55 in pyrimidine biosynthesis, is required for NAD(+) biosynthesis in place of the missing QPRTase.

56 hus, we investigated the presence of de novo NAD(+) biosynthesis in this organism.

57 bstantial efforts have been made to identify NAD(+) biosynthesis inhibitors, specifically against nic

58 NAD(+) biosynthesis is an attractive and promising thera

59 for a conserved phosphoribosyltransferase in NAD(+) biosynthesis.

60 eath signaling cascade involving loss of the NAD(+) biosynthetic enzyme Nmnat/Nmnat2 in axons, activa

61 factors, the most important of which is the NAD(+) biosynthetic enzyme NMNAT2 that inhibits activati

62 iling heart, we quantified the expression of NAD(+) biosynthetic enzymes in the human failing heart a

63 ditis elegans are reported to lack a de novo NAD(+) biosynthetic pathway.

64 creates novel possibilities for manipulating NAD(+) biosynthetic pathways, which is key for the futur

65 benefit requires a complete understanding of NAD(+) biosynthetic pathways.

66 Efficiency of initiation with NAD+, but not with UDP-containing factors, is affected b

67 Reduction of NAD(+) by dehydrogenase enzymes to form NADH is a key co

68 te medium, peroxisomal NADH is reoxidised to NAD(+) by malate dehydrogenase (Mdh3p) and reduction equ

69 yotes and raise the possibility that this 5' NAD(+) cap could modulate RNA stability and translation

70 a 5' end nicotinamide adenine dinucleotide (NAD(+)) cap that, in contrast to the m(7)G cap, does not

71 -capped mRNA levels and enables detection of NAD(+)-capped intronic small nucleolar RNAs (snoRNAs), s

72 Removal of DXO from cells increases NAD(+)-capped mRNA levels and enables detection of NAD(+

73 NADding enzyme modulating cellular levels of NAD(+)-capped RNAs.

74 c small nucleolar RNAs (snoRNAs), suggesting NAD(+) caps can be added to 5'-processed termini.

75 XO/Rai1 decapping enzymes efficiently remove NAD(+) caps, and cocrystal structures of DXO/Rai1 with 3

76 ATP, but not NAD(+), causes a conformational shift to a less compact

77 se SDRs appear to contain a non-exchangeable NAD cofactor and may rely on an external redox partner,

78 erial SDRs in which the insertion buries the NAD cofactor except for a small portion of the nicotinam

79 As mice age and NAD(+) concentrations decline, DBC1 is increasingly boun

80 To determine whether a Nampt-NAD(+) control system exists within the aortic media and

81 To determine whether a Nampt-NAD(+) control system in SMCs impacts aortic integrity,

82 In null mice, the prevention of NAD deficiency during gestation averted defects.

83 ryos of Haao-null or Kynu-null mice owing to NAD deficiency.

84 NAD + dependent Sirtuin 6 (SIRT6) is a glucose homeostas

85 e successful detection of formaldehyde using NAD(+) dependent formaldehyde dehydrogenase.

86 Sirtuins are NAD(+) dependent protein deacetylases, which are involve

87 gs additionally support a role for decreased NAD(+) dependent Sirt6 activity in mediating dioxin toxi

88 ide adenine dinucleotid (NADH) ratio and the NAD(+)-dependent deacetylase activity of sirtuin 3 to in

89 NAD(+) and ATP synthesis linked to a loss of NAD(+)-dependent deacetylase activity, increased protein

90 f cancer invasion by OGT is dependent on the NAD(+)-dependent deacetylase SIRT1.

91 he ultimate step in lysine biosynthesis, the NAD(+)-dependent dehydrogenation of saccharopine to lysi

92 igase family (T4 RNA ligase 1; Rnl1) and the NAD(+)-dependent DNA ligase family (Escherichia coli Lig

93 Because parasitic Zn(2+)- and NAD(+)-dependent HDACs play crucial roles in the modulat

94 phosphorylation, we explored the role of the NAD(+)-dependent lysine deacetylase, sirtuin 1 (SIRT1) i

95 ow that the Dtx3L/Parp9 heterodimer mediates NAD(+)-dependent mono-ADP-ribosylation of ubiquitin, exc

96 f 19 ALDH superfamily members, catalyzes the NAD(+)-dependent oxidation of aldehydes to their respect

97 boosted NAD(+) levels and partially reversed NAD(+)-dependent phenotypes caused by mutation of pnc-1,

98 nction linked to decreased expression of the NAD(+)-dependent protein deacetylase SIRT1.

99 Sirt1 is an NAD(+)-dependent protein deacetylase that regulates many

100 nce that SIRT1, the most conserved mammalian NAD(+)-dependent protein deacetylase, is critically invo

101 SIRT1, the most conserved mammalian NAD(+)-dependent protein deacetylase, plays a vital role

102 how Sirtuin 1 (SIRT1), a conserved mammalian NAD(+)-dependent protein deacetylase, senses environment

103 Sirtuins (Sirt1-Sirt7) are NAD(+)-dependent protein deacetylases/ADP ribosyltransfe

104 In mitochondria, the sirtuin SIRT5 is an NAD(+)-dependent protein deacylase that controls several

105 nation of saccharopine to lysine, is another NAD(+)-dependent reaction performed inside peroxisomes.

106 ROC is composed of at least two subunits of NAD(+)-dependent retinol dehydrogenase 10 (RDH10), which

107 ization Promoting Protein (TPPP/p25) and the NAD(+)-dependent tubulin deacetylase sirtuin-2 (SIRT2) p

108 that the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy senso

109 mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal

110 The NAD+-dependent protein deacetylase CobB can reverse both

111 The SIR complex comprises the NAD-dependent deacetylase Sir2, the scaffolding protein

112 Sirtuins (SIRTs) are NAD-dependent deacylases, known to be involved in a vari

113 Sirtuins (SIRT1-7) are NAD-dependent proteins with the enzymatic activity of de

114 eover, the stronger effect of NR compared to NAD(+) depends of axonal stress since in AxD induced by

115 l NAD(+), yet the identity of the underlying NAD(+)-depleting enzyme(s) is unknown.

116 ate, points to reduced oxidative flux due to NAD(+) depletion after beta-lapachone treatment of NQO1+

117 SARM1 is required in axons to promote axonal NAD(+) depletion and axonal degeneration after injury.

118 gene that is activated by energy stress and NAD(+) depletion in isolated rat cardiomyocytes.

119 NAD(+) depletion is a common phenomenon in neurodegenera

120 cts of this drug on energy metabolism due to NAD(+) depletion were never described.

121 d by restoring the abundance of NAD(+) Thus, NAD(+) directly regulates protein-protein interactions,

122 Furthermore, the MtHDH complex with His and NAD(+) displays the cofactor molecule situated in a way

123 However, relative affinity to NAD+ does not depend on the -1 base of the template stra

124 gic receptors are required for extracellular NAD(+) (eNAD(+)) to evoke biological responses, indicati

125 ted by GAD1, we monitored the cytosolic NADH:NAD(+) equilibrium in tumor cells.

126 cide substrate arabinosyl-2'-fluoro-2'-deoxy NAD(+) (F-araNAD(+)), dimeric F-araNAD(+), to induce hom

127 ration of nicotinamide adenine dinucleotide (NAD) falls, at least in part due to metabolic competitio

128 f an intact de novo biosynthesis pathway for NAD(+) from tryptophan via QA, highlighting the function

129 The aortic media depends on an intrinsic NAD(+) fueling system to protect against DNA damage and

130 ensor was developed via direct attachment of NAD(+)-glycerol dehydrogenase coenzyme-apoenzyme complex

131 hin the coding region of the essential gene, nadD, greatly reduces its transcriptional output in stat

132 s not observed in ndufs8.1 ndufs8 Similarly, NAD(H) content, which was higher in the SD condition in

133 e propose that altered redox homeostasis and NAD(H) content/redox state control the phenotype of CI m

134 expression of CtBP, or transfection with an NAD(H) insensitive CtBP, and are replicated by a synthet

135 s on the cytosolic NADH:NAD(+) ratio and the NAD(H) sensitive transcriptional co-repressor CtBP.

136 cts on the cytosolic NADH:NAD+ ratio and the NAD(H)-sensitive transcription co-repressor CtBP.

137 ydrate-based natural deep eutectic solvents (NADES) have extensive potential for this process.

138 To explore possible alterations of NAD(+) homeostasis in the failing heart, we quantified t

139 protection involves defending intracellular NAD(+) homeostasis.

140 trating contribution of de novo synthesis to NAD(+) homeostasis.

141 omoted microtubule assembly independently of NAD(+); however, the TPPP/p25-assembled tubulin ultrastr

142 of its substrate NMN rather than generating NAD; however, this is still debated.

143 de riboside, nicotinamide mononucleotide and NAD in milk by means of a fluorometric, enzyme-coupled a

144 ) cells, indicating a more oxidized state of NAD in the cytosol upon glucose stimulation.

145 The betaine monohydrate-glycerol NADES in a molar ratio of 1:8 was determined to be the p

146 at NR is a better neuroprotective agent than NAD(+) in excitotoxicity-induced AxD and that axonal pro

147 suggests that phenazines may substitute for NAD(+) in LpdG and other enzymes, achieving the same end

148 on the mechanisms regulating homeostasis of NAD(+) in the failing heart.

149 y dilated aortas that had a 43% reduction in NAD(+) in the media.

150 We observed a 30% loss in levels of NAD(+) in the murine failing heart of both DCM and trans

151 Mutations in LecRK-I.8 inhibit NAD(+)-induced immune responses, whereas overexpression

152 rtant for discriminating between NADP(+) and NAD(+) Interestingly, a T28A mutant increased the kineti

153 tself has intrinsic NADase activity-cleaving NAD(+) into ADP-ribose (ADPR), cyclic ADPR, and nicotina

154 During this process, NAD(+) is reduced to NADH.

155 response, nicotinamide adenine dinucleotide (NAD(+)) is emerging as a metabolic target in a number of

156 Nicotinamide adenine dinucleotide (NAD) is produced via de novo biosynthesis pathways and b

157 Nicotinamide adenine dinucleotide (NAD) is synthesized de novo from tryptophan through the

158 acologic inhibition of the metabolic enzymes NAD kinase or ketohexokinase was growth inhibitory in vi

159 which can be enzymatically phosphorylated by NAD(+) kinase and ATP or (tz) ATP to the corresponding N

160 NADPH pools that are controlled by cytosolic NAD(+) kinase levels and revealed cellular NADPH dynamic

161 chondrial nicotinamide adenine dinucleotide (NAD) kinase (NADK2, also called MNADK) catalyzes phospho

162 To distinguish the role of hepatocyte NAD levels from any systemic effects of NR, we generated

163 cycling of nicotinamide to maintain adequate NAD levels inside the cells.

164 In human milk, NAD levels were significantly affected by the lactation

165 des, with decreased glucose tolerance, liver NAD(+) levels and citrate synthase activity in offspring

166 ynurenine pathway intermediates also boosted NAD(+) levels and partially reversed NAD(+)-dependent ph

167 dioxin and the PARP inhibitor PJ34 increased NAD(+) levels and prevented both thymus atrophy and hepa

168 orta constriction, by stabilizing myocardial NAD(+) levels in the failing heart.

169 Both NAPRT and NAMPT increased intracellular NAD(+) levels.

170 acellular nicotinamide adenine dinucleotide (NAD) levels, thus preventing or ameliorating metabolic a

171 We show that NAD(+) loss is attributable to increased PARP activity i

172 epted model for dioxin toxicity, we identify NAD(+) loss through PARP activation as a novel unifying

173 olymerase 1 (PARP1) activity, low endogenous NAD(+), low expression of SIRT1 and PGC1alpha and low ad

174 1 as a critical transcriptional regulator of NAD(+) metabolism.

175 By contrast, the 1.55-A LigA*NAD(+)*Mg(2+) structure reveals a one-metal mechanism in

176 (AxD) much more strongly than extracellular NAD(+) Moreover, the stronger effect of NR compared to N

177 al encoded mRNAs in Saccharomyces cerevisiae NAD-mRNA appears to be produced cotranscriptionally beca

178 equivalents between the intramitochondrial [NAD(+) ]/[NADH] pool to molecular oxygen, with irreversi

179 modulated by the PO2 and intramitochondrial [NAD(+) ]/[NADH].

180 suggest that it helps readjust the cellular NAD(+)/NADH balance when perturbed by different stimuli.

181 ative block due to the inability to maintain NAD(+)/NADH homeostasis.

182 abolic indicators and metabolites: cytosolic NAD(+)/NADH ratio (inferred from the dihydroxyacetone ph

183 evels; and a role for a more oxidized state (NAD(+)/NADH) in the cytosol during GIIS that favors high

184 well as an overall decrease in mitochondrial NAD(+)/NADH.

185 photophysical behavior to that of the native NAD(+)/NADH.

186 ding sites are open to solvent, which allows NAD/NADH exchange to support multiple turnover.

187 The up-regulation of NAD/NADH phosphorylation and dephosphorylation pathway,

188 te [AMP], nicotinamide adenine dinucleotide /NAD, nicotinamide adenine dinucleotide phosphate / nicot

189 NADES opens interesting perspectives for their potential

190 adening and STD-NMR experiments did not show NAD or NADH exchange on the NMR timescale.

191 We show that NHDs are NAD(+) (oxidized form of nicotinamide adenine dinucleoti

192 to reflect a decrease in the activity of the NAD(+) (oxidized nicotinamide adenine dinucleotide)-depe

193 The results also emphasize the importance of NAD(P)(+) :NAD(P)H redox homeostasis and associated ATP:

194 n complex participating in the regulation of NAD(P)(+) :NAD(P)H redox homeostasis in various prokaryo

195 ly 2), demonstrates that it possesses potent NAD(P)(+) hydrolase activity.

196 electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)(+)) to drive metabolic transformations in and acr

197 immunity protein and found that it resembles NAD(P)(+)-degrading enzymes.

198 onize its competitors and broadly implicates NAD(P)(+)-hydrolyzing enzymes as substrates of interbact

199 lucose into monoterpenes that generates both NAD(P)H and ATP in a modified glucose breakdown module a

200 NfnII affects the cellular concentrations of NAD(P)H and particularly NADPH.

201 r recognition of the two cofactors, F420 and NAD(P)H by FNO.

202 y Nrf2 target genes (i.e., heme oxygenase-1, NAD(P)H dehydrogenase, quinone 1, glutathione reductase,

203 The chloroplast NAD(P)H dehydrogenase-like (NDH) complex consists of abo

204 NAD(P)H dehydrogenases comprise type 1 (NDH-1) and type

205 However, NAD(P)H FLIM has not been established as a metabolic pro

206 Furthermore, NAD(P)H fluorescence lifetime imaging revealed an increa

207 NAD(P)H fluorescence lifetime imaging showed that EPA ac

208 fetime imaging revealed an increase in bound NAD(P)H fraction upon Mn treatment for neurons, consiste

209 in PCa cells shows Trp-quenching due to Trp-NAD(P)H interactions, correlating energy transfer effici

210 metabolism show in response to doxorubicin, NAD(P)H mean fluorescence lifetime (taum) and enzyme-bou

211 Here we discover that NAD(P)H oxidase 4 (NOX4), an enzyme known to catalyse th

212 le factor-1alpha (HIF-1alpha), downstream of NAD(P)H oxidase-4 (NOX4)-derived reactive oxygen species

213 s-tat, a peptide that blocks the activity of NAD(P)H oxidase.

214 nd this was mediated by high levels of Nrf2, NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase-

215 also emphasize the importance of NAD(P)(+) :NAD(P)H redox homeostasis and associated ATP:ADP equilib

216 articipating in the regulation of NAD(P)(+) :NAD(P)H redox homeostasis in various prokaryotic and euk

217 ous NO inhibited respiration and reduced the NAD(P)H redox state, pyridine nucleotide redox states we

218 ymes also requires a regenerating system for NAD(P)H to avoid the costs associated with this natural

219 cotinamide adenine dinucleotide (phosphate) (NAD(P)H) and flavin adenine dinucleotide (FAD).

220 e optical redox ratio, defined as FAD/(FAD + NAD(P)H), revealed three distinct redox distributions an

221 se in PCa cells by tracking auto-fluorescent NAD(P)H, FAD and tryptophan (Trp) lifetimes and their en

222 cotinamide adenine dinucleotide (phosphate), NAD(P)H, has been previously exploited for label-free me

223 an enzyme known to catalyse the oxidation of NAD(P)H, is upregulated when p16 is inactivated by looki

224 t directly consume reducing equivalents from NAD(P)H, nor demonstrate nitroreductase activity.

225 elating energy transfer efficiencies (E%) vs NAD(P)H-a2%/FAD-a1% as sensitive parameters in predictin

226 D enzyme-bound (a1%) fraction was decreased, NAD(P)H-a2%/FAD-a1% FLIM-based redox ratio and ROS incre

227 zyme in proline biosynthesis, catalyzing the NAD(P)H-dependent reduction of Delta(1)-pyrroline-5-carb

228 se), and electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)(+)) to drive metabolic transformations in

229 educes the activity and stability in vivo of NAD(P)H:quinone oxidoreductase 1 (NQO1).

230 beta-Lapachone is bioactivated by NAD(P)H:quinone oxidoreductase 1 (NQO1).

231 increases the ROS level in cancer cells via NAD(P)H:quinone oxidoreductase-1 (NQO1) catalysis, which

232 ion was only partially restored by increased NAD/P levels.

233 increase in the intracellular pool of total NAD/P.

234 Nicotinamide adenine dinucleotide (NAD(+)) participates in intracellular and extracellular

235 sion of neutrophil CXCR2, CD11b, and reduced NAD phosphate oxidase components (p22phox, p67phox, and

236 , we supplied nicotinamide riboside (NR), an NAD precursor, in the drinking water of mice subjected t

237 When supplied as the sole NAD precursor, quinolinate promoted B. bronchiseptica gr

238 ion of a diet with nicotinamide riboside, an NAD precursor, replenished hepatic NADP and protected th

239 Oral administration of the NAD(+) precursor nicotinamide (vitamin B3), and/or gene

240 We studied the impact of NAD(+) precursor supplementation on cardiac function in

241 We have shown that the NAD(+) precursor, nicotinamide mononucleotide (NMN) can

242 de riboside, the most energy-efficient among NAD precursors, could be useful for treatment of heart f

243 Pharmacological ascorbate depleted cellular NAD+ preferentially in cancer cells versus normal cells,

244 therapy (driving expression of Nmnat1, a key NAD(+)-producing enzyme), was protective both prophylact

245 phosphoribosyltransferase (NAPRT), a second NAD(+)-producing enzyme, is amplified and overexpressed

246 proven limited, suggesting that alternative NAD(+) production routes exploited by tumors confer resi

247 complexed with imidazole, HOL, and His with NAD(+) provided in-depth insights into the enzyme archit

248 The iron(IV) imide complexes, (Me2IPr)-R2Fe=NAd (R = (neo)Pe (3a), 1-nor (3b)) undergo migratory ins

249 tivity through effects on the cytosolic NADH:NAD(+) ratio and the NAD(H) sensitive transcriptional co

250 Changes in the NADH:NAD(+) ratio regulate CtBP binding to the acetyltransfer

251 educed glucose availability reduces the NADH:NAD(+) ratio, NF-kappaB transcriptional activity, and pr

252 g mice, suggestive of a shift in tissue NADH/NAD(+) ratio.

253 ponses through effects on the cytosolic NADH:NAD+ ratio and the NAD(H)-sensitive transcription co-rep

254 tive with a variety of substrates: ((Ar)L)Fe(NAd) reacts with azide yielding a ferrous tetrazido ((Ar

255 of peripheral neuropathy, stimulated tissue NAD recovery, improved general health, and abolished att

256 K activity, Akt activity, and cytosolic NADH/NAD(+) redox state were temporally linked in individual

257 K activity, Akt activity, and cytosolic NADH/NAD(+) redox.

258 lating nicotinamide adenine dinucleotide(+) (NAD(+))/reduced form of nicotinamide adenine dinucleotid

259 t intracortical administration of NR but not NAD(+) reduces brain damage induced by NMDA injection.

260 f O2 -tolerant hydrogen cycling by a soluble NAD(+) -reducing [NiFe] hydrogenase, we herein present t

261 Thus, alternative routes for NAD regeneration must exist to support the increased gly

262 shuttle, which is important for cytoplasmic NAD(+) regeneration that sustains rapid glucose breakdow

263 by distinct circadian hepatic signatures in NAD(+)-related metabolites and cyclic global protein ace

264 lular RNAs being 'capped' at the 5' end with NAD+, reminiscent of eukaryotic cap.

265 Strikingly, treatment in vivo with the NAD(+) repleting agent nicotinamide, a form of vitamin B

266 Regeneration of the NAD required to support enhanced glycolysis has been att

267 de that the availability of intraperoxisomal NAD(+) required for saccharopine dehydrogenase activity

268 cribed 5' nicotinamide-adenine dinucleotide (NAD(+)) RNA in bacteria.

269 Whether 5' NAD-RNA exists in eukaryotes remains unknown.

270 s to be produced cotranscriptionally because NAD-RNA is also found on pre-mRNAs, and only on mitochon

271 We demonstrate that 5' NAD-RNA is found on subsets of nuclear and mitochondrial

272 which encodes a nicotinamidase required for NAD(+) salvage biosynthesis, demonstrating contribution

273 icotinamide phosphoribosyltransferase in the NAD(+) salvage pathway.

274 e influx, the pentose phosphate pathway, and NAD salvaging pathways.

275 NAD(+)-sensitive pathways, such as glycolysis, flux thro

276 promized mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1alpha axis.

277 of supplied pyridines, indicative of de novo NAD synthesis and functional confirmation of Bordetella

278 Disruption of NAD synthesis caused a deficiency of NAD and congenital

279 bosyltransferase, a rate-limiting enzyme for NAD synthesis, specifically in the liver.

280 inamide or nicotinic acid, respectively, for NAD synthesis.

281 NADES synthesis as well as the extraction procedures wer

282 Nicotinamide riboside efficiently rescues NAD(+) synthesis in response to FK866-mediated inhibitio

283 NMN-consuming activity with NMNAT2, but not NAD-synthesizing activity, and it delays axon degenerati

284 Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive.

285 In patients with AD vs those with NAD, the myeloid compartment showed an increased CD11b (

286 izes in the presence of a proline analog and NAD(+) These results are consistent with the morpheein m

287 pidly reversed by restoring the abundance of NAD(+) Thus, NAD(+) directly regulates protein-protein i

288 elease and hydrolysis of ATP, cAMP, AMP, and NAD to adenosine.

289 o called MNADK) catalyzes phosphorylation of NAD to yield NADP.

290 It metabolizes NAD(+) to adenosine diphosphate ribose (ADPR) and cyclic

291 t description of extracellular conversion of NAD(+) to NR prompted us to probe the effects of NAD(+)

292 The binding of NAD(+) to the NHD domain of DBC1 (deleted in breast canc

293 rases use nicotinamide adenine dinucleotide (NAD(+)) to modify target proteins with ADP-ribose.

294 uction of nicotinamide adenine dinucleotide (NAD(+)) via nicotinamide phosphoribosyltransferase (Namp

295 The selectivity of these NADES was determined to select a preferable solvent.

296 occurs in multiple neurologic disorders and NAD(+) was shown to prevent neuronal degeneration in thi

297 scription with adenosine-containing cofactor NAD+, which was proposed to result in a portion of cellu

298 tracellular lectin domain of LecRK-I.8 binds NAD(+) with a dissociation constant of 436.5 +/- 104.8 n

299 1 activity and was reversible on resupplying NAD(+) with nicotinamide riboside.

300 thway that culminates in depletion of axonal NAD(+), yet the identity of the underlying NAD(+)-deplet