ライフサイエンスコーパス: NADP

1 NADP networks responded to this complex disaster, and pr

2 NADP(+) impairs ADP-ribosylation-dependent DNA damage re

3 NADP(+) is reduced back to NADPH by activation of mitoch

4 NADP(H) is an essential cofactor of multiple metabolic p

5 NADP-malic enzyme (ME), the most widespread C(4) decarbo

6 NADP-MDH is a strictly redox-regulated, light-activated

7 NADP-ME2 is the only one located in the cell cytosol of

8 osition over North America were made for 167 NADP sites before and after the Fukushima Dai-ichi Nucle

9 y different from the ubiquitous co-enzyme 2'-NADP and the calcium mobilizer 2'-NAADP.

10 ponsive genes such as proline transporter 2, NADP-dependent glyceraldehyde and superoxide dismutase w

11 Both products of AvrRxo1, 3'-NADP and 3'-nicotinic acid adenine dinucleotide phosphat

12 Interestingly, 3'-NADP and 3'-NAADP have previously been used as inhibitor

13 and cocrystal structures of DXO/Rai1 with 3'-NADP(+) illuminate the molecular mechanism for how the "

14 how that regulation of maize (Zea mays) C(4)-NADP-ME activity is much more elaborate than previously

15 hosphorylation of the Ser419 residue of C(4)-NADP-ME in protein extracts of maize leaves.

16 Analysis of the crystal structure of C(4)-NADP-ME indicated that Ser419 is involved in the binding

17 We propose that phosphorylation of ZmC(4)-NADP-ME at Ser419 during the first hours in the light is

18 Phosphorylation of ZmC(4)-NADP-ME drastically decreases its activity as shown by t

19 ive oxygen species, total glutathione, and a NADP(+)/NADPH ratio than wild-type cells under limiting

20 ate, thus regenerating the electron acceptor NADP.

21 kinetic isotope effects (KIEs) accompanying NADP(+) reduction by dehydrogenases and transhydrogenase

22 The AKR1C3.NADP(+).2'-des-methyl-indomethacin crystal structure was

23 In alpha-NADP-ME plants with less than 40% of wild-type NADP-ME a

24 The comparison of alpha-NADP-ME and antisense Rubisco small subunit demonstrates

25 iols to solutions of NBT plus beta- or alpha-NADP did not produce diformazan, (5) S-nitrosothiols did

26 Transgenic plants (alpha-NADP-ME) exhibited a 34% to 75% reduction in NADP-ME act

27 h key limitations of A(n) , especially among NADP-ME species.

28 EryKR1 in the presence of a catalytic amount NADP(+) (0.05 equiv) resulted in time- and cofactor-depe

29 Evolution from an NADP(+) to a bispecific NADP(+) and CoA binding site inv

30 ht thioredoxin reductases (LMW TrxRs), is an NADP(+)-independent dithiol oxidase.

31 Here we report the discovery of an NADP(H)-dependent reductive aminase from Aspergillus ory

32 ere not detectable for its chemical analogue NADP and were blocked by the NAADP antagonist trans-Ned-

33 how that the interaction between Ser-257 and NADP(H) is essential for stabilization of the C4a-hydrop

34 lls, and hypoxia elicited both aconitase and NADP(+)-isocitrate dehydrogenase activity losses.

35 X-ray crystal structures of apo- and NADP(+)-bound selected mutants show that the substrate-b

36 The overall architecture and NADP(+)-binding site of Tfu-FNO were highly similar to t

37 FMO signature sequence, and FAD-binding and NADP-binding sequences.

38 3'- and 2'-ribose phosphate group of CoA and NADP(+), respectively, but a different one for the commo

39 dox-active, nonepimerizing EryKR6 domain and NADP(+) resulted in time- and cofactor-dependent washout

40 NAD(H) binds to a-FAD and NADP(H) consequently to b-FAD, which is positioned in th

41 ird substrate, in addition to ferredoxin and NADP(H), is as yet unknown.

42 crease in the reductive states of NAD(H) and NADP(H) redox systems.

43 t NOCT can regulate levels of both mRNAs and NADP(H) cofactors in a manner specified by its location

44 uces a severe attack on host cell NAD(+) and NADP(+) Finally, we show that NAMPT activation, NAM, and

45 y 50% within 24 h; concomitantly, NAD(+) and NADP(+) increase proportionately; however, degassing the

46 The pyridine nucleotides NAD(+) and NADP(+) play a pivotal role in regulating intermediary m

47 In general, NAD(+) and NADP(+) receive electrons to become NADH and NADPH by co

48 Both Fdx1-dependent reductions of NAD(+) and NADP(+) were cooperative.

49 iversally essential dinucleotides NAD(+) and NADP(+).

50 fructose 6-phosphate and oxidised (NAD+ and NADP+) and reduced (NADH) nicotinamide dinucleotides, wh

51 -MDH, confirming distinct roles for NAD- and NADP-linked redox homeostasis.

52 ton gradient to generate NADPH from NADH and NADP(+), provides the link between mitochondrial respira

53 nderstanding of the roles of NAD(+)/NADH and NADP(+)/NADPH in cellular physiology and pathology could

54 view the multiple actions of NAD(+)/NADH and NADP(+)/NADPH in regulating intermediary metabolism in t

55 cating that the rate constants for NADPH and NADP(+) dissociation were greatly enhanced relative to t

56 e adenine dinucleotide phosphate (NADPH) and NADP(+) are cycled rapidly between ferredoxin-NADP(+) re

57 ocesses between Anabaena FNR(rd)/FNR(ox) and NADP(+)/H, accounting also for the solvation.

58 ependent small molecule dithiol oxidases and NADP(+)-dependent thioredoxin reductases and provide ins

59 ary to drive water oxidation into oxygen and NADP(+) reduction into NADPH with visible light.

60 temperature was less pronounced for PCK and NADP-ME Rubisco, which would be advantageous in warmer c

61 The crystal structures of ribose and NADP(+) (the oxidized form of nicotinamide adenine dinuc

62 d by antioxidant enzymes, reduced thiols and NADP(H) cofactors, which is critical for cancer cells su

63 ermediate adduct of finasteride and NADPH as NADP-dihydrofinasteride in a largely enclosed binding ca

64 3) the addition of enzyme cofactors such as NADP(H) was not necessary.

65 tios led to increased nitrogen assimilation, NADP-malate dehydrogenase activation, and light vulnerab

66 observations explain the difference between NADP(+)-independent small molecule dithiol oxidases and

67 -55 are important for discriminating between NADP(+) and NAD(+) Interestingly, a T28A mutant increase

68 After TMA binding, NADP(+) bends and interacts with D317, shutting off the

69 Evolution from an NADP(+) to a bispecific NADP(+) and CoA binding site involves many amino acid ex

70 m in complex with NADP(H) and also with both NADP(H) and the pharmaceutical ingredient (R)-rasagiline

71 Pen contains strongly bound NADP(+) and has distinct UDP-GlcNAc 4-oxidase, 5,6-dehyd

72 only precipitation samples were collected by NADP and analyzed for fission-product isotopes within wh

73 boxylation by IDH1 was potently inhibited by NADP(+) and, to a lesser extent, by ICT.

74 step in lysine degradation are performed by NADP-dependent oxidoreductases explaining their in vivo

75 NAD was replaced by NADP.

76 NAD/NADP was replaced by NADP/NADPH.

77 dinucleotide phosphate, reduced are used by NADP-dependent malate dehydrogenase (MDH) to reduce OAA

78 Arabidopsis thaliana) protein that catalyzes NADP(+) production exclusively in the presence of CaM/Ca

79 , contributes to an increase in the cellular NADP(+) concentration and to the amplification of the el

80 hermotoga maritima from its natural coenzyme NADP(+) to NAD(+).

81 ate a less favorable binding of the cofactor NADP in the phosphomimetic and the phosphorylated varian

82 uent dark reactions, which include cofactor (NADP(+)) release and cofactor (NADPH) rebinding, show di

83 to convert malate to pyruvate and to convert NADP(+) to NADPH; the NADPH is detected spectrometricall

84 l isocitrate dehydrogenase 2 (IDH2) converts NADP(+) to NADPH and promotes regeneration of reduced gl

85 ctivity toward the dinucleotide 2',3'-cyclic NADP.

86 Point mutations at Arg132 of the cytoplasmic NADP(+)-dependent isocitrate dehydrogenase 1 (IDH1) occu

87 the pentose phosphate pathway, but cytosolic NADP(+)-dependent dehydrogenases using intermediates of

88 Upon IL8 stimulation, cytosolic NADP(+) is transported to acidified endolysosomes via co

89 Mutations in the cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDH1) occur

90 citrate/isocitrate carrier and the cytosolic NADP-dependent isocitrate dehydrogenase (ICDc), is invol

91 The alternative malate decarboxylase, NADP-ME, did not appear to compensate for the reduction

92 ind that NOCT increases NAD(H) and decreases NADP(H) levels in a manner dependent on its intracellula

93 Ectopic AOX1 expression decreases NADP production, PPP flux and nucleotide synthesis, whil

94 cal data indicate that NOCT dephosphorylates NADP(H) metabolites, and thus we measured the effect of

95 ins are involved in cellular detoxification, NADP metabolism, glutathione metabolism and the electron

96 eukaryotic and bacterial UGMs have different NADP(H) binding sites.

97 cally and directly converts the dinucleotide NADP(+) into NAD(+) and NADPH into NADH.

98 , we show that NOC utilizes the dinucleotide NADP(H) as a substrate, removing the 2' phosphate to gen

99 han-kynurenine pathway resulting in elevated NADP levels which may increase metabolic flux through th

100 , increase eNOS protein content and the eNOS/NADP(H)oxidase protein ratio in previously sedentary lea

101 encoding the key nitrogen metabolism enzyme NADP-glutamate dehydrogenase.

102 e dinucleotide (NAD) phosphate malic enzyme (NADP-ME) and phosphoenolpyruvate carboxykinase (PCK) pho

103 A. thaliana contains four malic enzymes (NADP-ME 1-4) to catalyze the reversible oxidative decarb

104 hesize NAADP by base exchange from exogenous NADP and nicotinic acid and metabolize exogenous NAADP t

105 tead, it exhibits non-bifurcating ferredoxin NADP oxidoreductase-type activity.

106 fibroblast cells showed deficient ferredoxin NADP reductase activity and mitochondrial dysfunction ev

107 elated bifurcating NADH-dependent ferredoxin NADP(+) oxidoreductase (NfnI).

108 lavin-based enzyme NADH-dependent ferredoxin NADP(+) oxidoreductase I (NfnI) from the hyperthermophil

109 ivity by using an assay employing ferredoxin NADP(+) reductase (FNR) to transfer electrons from NADPH

110 r a unique pair of ferredoxin and ferredoxin-NADP(+) reductase isoforms.

111 Hydrogenases, ferredoxins, and ferredoxin-NADP(+) reductases (FNR) are redox proteins that mediate

112 n for reduced ferredoxins between ferredoxin-NADP(+) oxidoreductase and hydrogenases, rather than due

113 ADP(+) are cycled rapidly between ferredoxin-NADP(+) reductase and a second enzyme-the pairs being ju

114 dependent and can be mediated by ferredoxin-NADP(+) reductase (FNR) in vitro.

115 2S] ferredoxin (PetF), reduced by ferredoxin-NADP(+) reductase (FNR) using NADPH, has been implicated

116 lly in bifurcating NADH-dependent ferredoxin-NADP(+) oxidoreductase and the non-bifurcating flavoprot

117 ASQ of bifurcating NADH-dependent ferredoxin-NADP(+) oxidoreductase I and can be an indication of cap

118 A merodiploid ferredoxin-NADP reductase mutant produced correspondingly more phot

119 During photosynthesis, ferredoxin-NADP(+) reductase (FNR) catalyzes the electron transfer

120 (Arabidopsis thaliana) leaf-type FERREDOXIN-NADP(+) OXIDOREDUCTASE (FNR) isoforms, the key enzymes l

121 f FinR regulation, fprA (encoding ferredoxin:NADP(+) oxidoreductase), or by Escherichia coli cysJI (e

122 The enzyme ferredoxin:NADP(+) reductase (FNR) has the potential to regulate th

123 NADH-dependent reduced ferredoxin:NADP oxidoreductase (NfnAB) is found in the cytoplasm of

124 lysis disclosed that ferredoxin (flavodoxin):NADP(+) oxidoreductase could use NADH to reduce Fd and t

125 tochondrial NAD kinase, which is crucial for NADP biosynthesis evidenced by decreased mitochondrial N

126 cks a conserved GGGDXAXE motif necessary for NADP(+) binding in the canonical LMW TrxRs, but also con

127 nzymes, adopting a different orientation for NADP binding and offer a structural framework for design

128 CD38, a signal-mediated transport system for NADP(+) and luminal NAD(+) biosynthetic enzymes integrat

129 In contrast, its phosphorylated form, NADP, plays a central role in biosynthetic pathways and

130 P, thereby decoupling ribose biogenesis from NADP/NADPH-mediated redox control.

131 ld reversal of the coenzyme selectivity from NADP(+) to NAD(+).

132 tica with reversed coenzyme selectivity from NADP(+) to NAD(+).

133 8-fold reversal of coenzyme selectivity from NADP(+) to NAD(+).

134 , the only enzyme responsible for generating NADP, which is rapidly converted to NADPH by dehydrogena

135 ion of the cofactor is enhanced in the E.GMP.NADP(+) complex.

136 inct interactions in E.IMP.NADP(+) and E.GMP.NADP(+) complexes.

137 This work indicates that animal NADKs govern NADP biosynthesis in vivo and are regulated by evolution

138 adk, an NAD(+) kinase-encoding gene, governs NADP biosynthesis in vivo and is essential for developme

139 The ternary complex structure of hAR*NADP(+)*WY 14,643 reveals the first structural evidence

140 dissociation constants, Kd, of oxidized (hAR*NADP(+)) and reduced (hAR*NADPH) holoenzyme complexes di

141 ociation of WY 14,643 from the oxidized (hAR*NADP(+)*WY 14,643) and reduced (hAR*NADPH*WY 14,643) ter

142 oside, an NAD precursor, replenished hepatic NADP and protected the mice from hepatotoxicity, based o

143 tative metabolomics established that hepatic NADP(+) and NADPH levels were significantly degraded in

144 ls regulate their NADP pools in vivo and how NADP-synthesizing enzymes are regulated have long remain

145 ctivity of TNT and found that TNT hydrolyzes NADP(+) as fast as NAD(+) but does not cleave the corres

146 Taken together, our study identifies NADP(+) as an endogenous PARP inhibitor that may have im

147 osphates have distinct interactions in E.IMP.NADP(+) and E.GMP.NADP(+) complexes.

148 Furthermore, improved NADP-dependent HPR1 activities in peroxisomes could not

149 The latter can be engaged in NADP-specific coupled enzymatic transformations involvin

150 Fumarate produced an increase in NADP-ME2 activity by binding to an allosteric site.

151 NADP-ME) exhibited a 34% to 75% reduction in NADP-ME activity relative to the wild type with no visib

152 of NADK stimulates its activity to increase NADP(+) production through relief of an autoinhibitory f

153 atabolism, (b) decreased NADPH and increased NADP(+) levels, and (c) decreased basal, spare, and maxi

154 ls and directly in vitro, thereby increasing NADP(+) production.

155 straints of the CoA structure also influence NADP(+) binding.

156 for a sufficient provision of intracellular NADP(+) with the activity of NAD kinase (NADK).

157 The intracellular NADP(+)/NADPH ratio controls flux through the pentose ph

158 1, in which the labels 'NADP(+)' and 'NADPH + H(+)' were incorrectly given as 'N

159 peroxide anion production, ATP drop and late NADP(H) depletion associated with a mitochondrial induce

160 a simple purge valve module for maintaining NADP(+)/NADPH balance.

161 th hyperlysinemia is caused by mitochondrial NADP(H) deficiency due to a mutation in NADK2.

162 nthesis evidenced by decreased mitochondrial NADP(H) levels in patient fibroblasts.

163 specific function of Pos5p in mitochondrial NADP(+) and NADPH biosynthesis.

164 s known about the functions of mitochondrial NADP and MNADK in liver physiology and pathology.

165 tigated the effects of reduced mitochondrial NADP by deleting MNADK in mice.

166 bly those involved in peptidoglycan monomer, NADP(+), heme, lipid, and carotenoid biosynthesis) or PM

167 genes for the synthesis of nicotinate, NAD+, NADP+ and coenzyme A were detected among the essential v

168 ox couples in the mitochondrial matrix (NAD, NADP, thioredoxin, glutathione, and ascorbate) are in ki

169 NAD/NADP was replaced by NADP/NADPH.

170 -G along with redox coenzymes (NAD(+), NADH, NADP(+), NADPH), energy coenzymes (ATP, ADP, AMP), antio

171 including glycocholate, fatty acids, NADPH, NADP+, some amino acids, thymidine, trigonelline, nicoti

172 2',7'-dichlorofluorescein diacetate), NADPH, NADP(+) and ATP contents (spectrophotometry), matrix met

173 The subsequent increase in NADPH-NADP(+) and ATP-ADP ratios led to increased nitrogen ass

174 NADPH/NADP(+) (the reduced form of NADP(+)/nicotinamide adenin

175 itochondrial membrane, establishing an NADPH/NADP(+) ratio severalfold higher than the NADH/NAD(+) ra

176 sulin secretion, the ATP/ADP ratio and NADPH/NADP(+) ratio.

177 isozyme resulted in decreased cellular NADPH/NADP(+) and reduced/oxidized glutathione ratios (GSH/GSS

178 his ROS formation and doubled cellular NADPH/NADP(+) ratio and ATP content.

179 four main redox couples (NADH/NAD(+), NADPH/NADP(+), GSH/GSSG, Trx(SH)(2)/TrxSS).

180 of the cytosolic region that regulate NADPH/NADP(+) exchange.

181 en pyruvate, ostensibly increasing the NADPH/NADP(+) ratio which can potentially maintain the cellula

182 he crystal structures of STMO in the native, NADP(+)-bound, and two mutant forms reveal structural de

183 A, and malonyl-CoA, as well as NADPH but not NADP(+), NADH, or NAD(+), act as allosteric activators o

184 of a microRNA-insensitive pdNAD-MDH but not NADP-MDH, confirming distinct roles for NAD- and NADP-li

185 unt we demonstrate that Gcd1 encodes a novel NADP(+)-dependent glucose dehydrogenase that acts in a p

186 release was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors o

187 Through amino acid-sequence alignment of NADP(+)- and NAD(+)-preferred 6PGDH enzymes and computer

188 ed that Ser419 is involved in the binding of NADP at the active site.

189 the key residues involved in the binding of NADP(+) and L-AHG and the catalysis are revealed.

190 Binding of NADP(+) to Kvbeta removes N-type inactivation of Kv curr

191 ence which physically impedes the binding of NADP(+).

192 ional changes associated with the binding of NADP(H) and l-ornithine.

193 at either flavin reduction or the binding of NADP(H) is sufficient to drive the FAD to the in conform

194 ulates local intracellular concentrations of NADP(H) in a manner that changes over the course of the

195 NADPH/NADP(+) (the reduced form of NADP(+)/nicotinamide adenine dinucleotide phosphate) hom

196 te between the reduced and oxidized forms of NADP independently of its catalytic activity and underwe

197 sponsible for binding the phosphate group of NADP(+) were identified.

198 Inhibition of NADP synthesis rescues the metabolic effects of AOX1 KD.

199 ense construct targeting the C(4) isoform of NADP-malic enzyme (ME), the primary enzyme decarboxylati

200 at ovarian cancer cells with higher level of NADP(+), an NAD(+) derivative, are more sensitive to PAR

201 a pivot point, allowing the nicotinamide of NADP(+) to slide into position for stabilization of the

202 esidues interacting with the 2'-phosphate of NADP(+) were probed by targeted mutagenesis, indicating

203 te of CoA aligns with the alpha-phosphate of NADP(+).

204 uctase, with almost identical positioning of NADP, Lys146(147), Tyr178(179), and F342(343), but only

205 X-ray structure of TbFolD in the presence of NADP(+) and the inhibitor, which then guided the rationa

206 The presence of NADP(+) is essential for activity, as it is required for

207 decarboxylation of malate in the presence of NADP.

208 ethod is also suitable for quantification of NADP(+) and NADPH.

209 olide B synthase and catalytic quantities of NADP(+) in the presence of redox-inactive, recombinant N

210 -tetrahydrofolate is coupled to reduction of NADP(+) to NADPH.

211 the oxidation of water and the reduction of NADP+, respectively.

212 umulated metabolites and the regeneration of NADP(+) from NADPH during poly-3-hydroxybutanoate synthe

213 dom substrate binding and ordered release of NADP(+) followed by MEP.

214 nicotinamide ring and the adjacent ribose of NADP(+), while the remainder of the enzyme is represente

215 ncipient HO(*) and O3' of the ribose ring of NADP(+) in the transition state for lysine.

216 The binding of the nicotinamide ring of NADP(+) is shifted with respect to the flavin compared w

217 termine the molecular details of the role of NADP(H) in catalysis, we targeted Ser-257 for site-direc

218 PI3K)-Akt pathway induces acute synthesis of NADP(+) and NADPH.

219 solic enzyme that catalyzes the synthesis of NADP(+) from NAD(+) (the oxidized form of NADH), on thre

220 The final effect of this metabolite on NADP-ME2 forward activity not only depends on fumarate a

221 and oxygen as cosubstrates, and produce only NADP(+) and water as byproducts, making them environment

222 ydrogenase activity can use either NAD(+) or NADP(+) but requires both phosphate and Mg(2+) when usin

223 trahydrofolate (THF), and cofactor (NADPH or NADP(+)).

224 and the exquisite selectivity of NADPH over NADP(+), NADH, and NAD(+) as an HDAC activator reveal a

225 Experimental structures of the FNR(ox):NADP(+) interaction have suggested a series of conformat

226 e and pyrimidine intermediates, and oxidized NADP(+) , accumulated in Deltandk1.

227 by increasing the amount of ATP produced per NADP(+) molecule reduced(4,5).

228 nicotinamide adenine dinucleotide phosphate (NADP(+) ) for the NA group of nicotinic acid adenine din

229 nicotinamide adenine dinucleotide phosphate (NADP(+) and NADPH), and adenosine triphosphate (ATP) and

230 nicotinamide adenine dinucleotide phosphate (NADP(+) and NADPH); coenzymes of energy including adenos

231 Nicotinamide adenine dinucleotide phosphate (NADP(+)) is essential for producing NADPH, the primary c

232 Nicotinamide adenine dinucleotide phosphate (NADP) is a critical cofactor during metabolism, calcium

233 ylated (NAD(+) and NADH) and phosphorylated (NADP(+) and NADPH) forms.

234 sses in all living organisms, and in plants, NADP(H) is required as the substrate of Ca(2+)-dependent

235 pyruvate carboxykinase (PEPCK) and plastidic NADP-dependent malic enzyme (ME) on tomato (Solanum lyco

236 rongly reduced levels of PEPCK and plastidic NADP-ME were generated by RNA interference gene silencin

237 malic enzyme (ME) and/or cytosolic/plastidic NADP-ME combined with the cytosolic/plastidic pyruvate o

238 eled glucoses of fruits lacking in plastidic NADP-ME and cytosolic PEPCK activities revealed differen

239 On the other hand, the plastidic NADP-ME antisense lines were characterized by no changes

240 Depletion of the NADPH precursor, NADP(+), coincided with formation of 2'-phospho-ADP ribo

241 Inhibition of CD38 prevented NADP(H) depletion and preserved endothelium-dependent re

242 the National Atmospheric Deposition Program (NADP), numerous measurements of radionuclide wet deposit

243 Acetylation at K76 and K294 of 6PGD promotes NADP(+) binding to 6PGD and formation of active 6PGD dim

244 ox(TM) Green Cytotoxicity, CellTiter-Glo(R), NADP/NADPH-Glo(TM), ROS-Glo(TM)/H(2)O(2), GSH/GSSG-Glo(T

245 prior to and upon hydride transfer, FNR(rd)-NADP(+) and FNR(ox)-NADPH, regardless of the hydride tra

246 s to extract electrons from water and reduce NADP(+) to NADPH.

247 te, develops within 120 minutes in a reduced NADP (NADPH) oxidase-dependent manner.

248 ) were critical for matching ATP and reduced NADP demand in BS and M when light capture was varied un

249 Leukocyte reduced NADP (NADPH) oxidase plays a key role in host defense an

250 de nucleotide transhydrogenase (NNT) reduces NADP(+) at the expense of NADH oxidation and H(+) moveme

251 We characterized the effect of reducing NADP-ME on photosynthesis by measuring in vitro photosyn

252 including NAD Kinase (NADK), which regulates NADP(H) homeostasis and cellular redox state.

253 ofactor in comparison to previously reported NADP(+)-bound structures, as the nicotinamide moiety is

254 Here we develop an approach to resolve NADP(H)-dependent pathways present within both the cytos

255 of GMP compared with IMP in their respective NADP(+) complexes.

256 NADPH reduces the flavin, and the resulting NADP(+) is the last product to be released.

257 ydrogenase 1 (IDH1) catalyzes the reversible NADP(+)-dependent conversion of isocitrate (ICT) to alph

258 ere measured at approximately 21% of sampled NADP sites distributed widely across the contiguous Unit

259 amination and the two decarboxylase systems (NADP-malic enzyme and phosphoenolpyruvate carboxykinase)

260 We demonstrate that NADP(+) acts as a negative regulator and suppresses ADP-

261 This finding fully supports the idea that NADP(H) adopts various positions during the catalytic cy

262 We showed previously that NADP appears to act as a trigger to kick the repressor o

263 T targeting to mitochondria and propose that NADP(H) regulation, which takes place at least in part i

264 by marine bacterial Tmm and first show that NADP(+) undergoes a conformational change in the oxidati

265 The NADP(+)-dependent dehydrogenase activity is inhibited by

266 The NADP(+)-dependent VvAHGD could efficiently oxidize L-AHG

267 crucial role of the Arg-329 residue and the NADP(+) cofactor for the catalytic efficiency of CHMO.

268 rogen bonds with the Arg-329 residue and the NADP(+) cofactor.

269 the pentose phosphate pathway (PPP) and the NADP-dependent malic enzyme (MEc).

270 itochondrial TRX pathway in Arabidopsis: the NADP-TRX reductase a and b double mutant (ntra ntrb) and

271 H) is a reversible enzyme that catalyzes the NADP(+)-dependent oxidative decarboxylation of isocitrat

272 fication of early-occurring mutations in the NADP(+)-dependent isocitrate dehydrogenase genes IDH1 an

273 ith the 2'-phosphate being pushed inside the NADP(+) binding domain instead of being stretched out in

274 alogous glioma-associated mutations into the NADP(+ )isocitrate dehydrogenase genes (IDP1, IDP2, IDP3

275 Moreover, the NADP(+) metabolite, NAADP(+), regulates intracellular ca

276 is structure shows a drastic rotation of the NADP(+) cofactor in comparison to previously reported NA

277 emia and reperfusion (I/R), depletion of the NADP(H) pool occurred and was most marked in the endothe

278 this rise by converting Hyperkinetic to the NADP(+)-bound form.

279 olo-TH is a highly asymmetric dimer with the NADP(H)-binding domain (dIII) in two different orientati

280 tive defense, yet how animals regulate their NADP pools in vivo and how NADP-synthesizing enzymes are

281 millisecond time scale motions for the E:THF:NADP(+) and E:THF:NADPH complexes of wild-type and the L

282 ns are highly correlated with fluxes through NADP(+)-reducing and NADPH-balancing reactions.

283 tivity by increasing its binding affinity to NADP(+) and therefore activates the PPP for NADPH and ri

284 zes the electron transfer from ferredoxin to NADP(+) via its FAD cofactor.

285 own cytosolic enzyme that converts NAD(+) to NADP(+), which is subsequently reduced to NADPH.

286 itors that alter the ratio of bound NADPH to NADP(+) (and hence the record of sleep debt or waking ti

287 abidopsis organs providing most of the total NADP-ME activity.

288 exhibits strong cofactor selectivity toward NADP(H).

289 DP-ME plants with less than 40% of wild-type NADP-ME activity, CO(2) assimilation rates at high inter

290 network for FDX1 and FDX2; and (d) in vitro NADP(+) reduction and H2 photo-production assays mediate

291 vealed an unexpected reaction cycle in which NADP(+) and CoA successively occupy identical binding si

292 While NADP(+) production in plants has long been known to invo

293 the substrate-free state and in complex with NADP(+) and CoA.

294 s of VvAHGD in the apo form and complex with NADP(+) and modeled its structure with L-AHG.

295 the crystal structure of FNO in complex with NADP(+) at 1.8 A resolution, providing the first bacteri

296 bstrate, the reduced enzyme, in complex with NADP(+), reacted with oxygen and formed an intermediate

297 ystal structures of AspRedAm in complex with NADP(H) and also with both NADP(H) and the pharmaceutica

298 sphogluconate into ribulose-5-phosphate with NADP(+) as cofactor in the pentose phosphate pathway (PP

299 the first structure of oxidized SidA without NADP(H) or l-ornithine bound (resting state).

300 K) catalyzes phosphorylation of NAD to yield NADP.