ライフサイエンスコーパス: NAD

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

2 NAD availability is limiting during liver regeneration,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 amate-cysteine ligase catalytic subunit, and NAD(P)H quinone oxidoreductase 1 in macrophages.

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

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

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

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

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

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

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

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

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

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

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

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

49 me and dose-dependent effects of NR on blood NAD(+) metabolism in humans.

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

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

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

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

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

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

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

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

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

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

60 e patients had reduced levels of circulating NAD.

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

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

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

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

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

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

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

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

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

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

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

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

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

74 forms of nicotinamide adenine dinucleotide (NAD(+) and NADH), oxidized and reduced forms of nicotina

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

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

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

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

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

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

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

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

83 egulating nicotinamide adenine dinucleotide (NAD) biosynthesis.

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

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

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

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

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

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

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

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

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

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

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

95 the redox status demonstrated that elevated NAD levels induce reactive oxygen species (ROS) producti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 anisms prioritize their use of pyridines for NAD biosynthesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 sults in combination with the role of NAM in NAD+ metabolism suggest an intriguing link between metab

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

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

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

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

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

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

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

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

140 protection involves defending intracellular NAD(+) homeostasis.

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

142 olinate-induced stimulation of intracellular NAD in transgenic nadC plants enhanced resistance agains

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 genes required for glutamine synthesis, NADH/NAD(P)H metabolism, as well as general DNA/RNA and amino

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

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

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

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

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

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

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

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

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

172 corresponding processes with the nonemissive NAD(+).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 DH-MDH and G6pDH-LDH) through the control of NAD(+) substrate channeling by specifically shifting NAD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 1 as a critical transcriptional regulator of NAD(+) metabolism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 1 activity and was reversible on resupplying NAD(+) with nicotinamide riboside.

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

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

235 ubstrate channeling by specifically shifting NAD(+) between the two enzyme pairs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 ncover an epigenetic program mediated by the NAD(+)-dependent histone deacetylase Sirtuin 6 (SIRT6) t

255 AMSDH catalyzes the NAD(+)-dependent oxidation of 2-aminomuconate semialdehy

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

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

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

259 the catalytic domain, thereby disrupting the NAD(+) and acetyl-lysine-binding sites.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 oute of electron transfer from ferredoxin to NAD.

284 of the coenzyme selectivity from NADP(+) to NAD(+).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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