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(+) is a competitive inhibitor with respect to NADPH

3 NADP(+) therefore is a likely regulator of O(2) and subs

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

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

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

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

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

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

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

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

12 ate, thus regenerating the electron acceptor NADP.

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

14 The structure of the AKR1D1.NADP(+)*finasteride complex determined at 1.7 A resoluti

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

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

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

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

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

20 rofolate to tetrahydrofolate and CO(2) in an NADP(+)-dependent reaction.

21 drofolate dehydrogenase (FDH, ALDH1L1) is an NADP(+)-dependent oxidoreductase and a structural and fu

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

23 rmophilic archaeon Pyrococcus furiosus is an NADP(H)-dependent heterotetrameric enzyme that contains

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

25 Importantly, S. viridis uses an NADP-malic enzyme subtype C(4) photosynthetic system to

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

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

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

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

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

31 35) loop movement controls NADPH binding and NADP(+) release; this loop movement in turn facilitates

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

33 3'- and 2'-ribose phosphate group of CoA and NADP(+), respectively, but a different one for the commo

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

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

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

37 ferredoxin:NADP(+)-oxidoreductase (FNR), and NADP(+).

38 ridine nucleotides (PNs), such as NAD(H) and NADP(H), mediate electron transfer in many catabolic and

39 ability to form alphaHG from isocitrate and NADP(+).

40 RDH10 can use both NAD(+) and NADP(+) as cofactors for 11-cis-RDH activity, although N

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 id (SA) or 3-DHS were used as substrates and NADP(+) as cofactor.

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

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

58 ith its substrate, cyclohexanone, as well as NADP(+) and FAD, to 2.4 A resolution.

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

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

61 -55 are important for discriminating between NADP(+) and NAD(+) Interestingly, a T28A mutant increase

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

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

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

65 xylatable substrate by the presence of bound NADP(+) (t((1/2)) = 33 min, 25 degrees C, pH 8).

66 s adjacent to the nicotinamide ring of bound NADP(+), Cys-707 and Glu-673, were replaced separately o

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

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

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

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

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

72 In most cases, NADP(+) formation significantly overestimated CYP1 catal

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

74 teraction of Anabaena FNR with its coenzyme, NADP(+).

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

76 All 12 residues that contact NADP(H) are conserved among eukaryotic UGMs.

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

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

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

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

81 Reducing cytosolic NADP-ME activity preferentially affected the sugar conte

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

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

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

85 els of NADP-linked isocitrate dehydrogenase (NADP-ICDH), glucose-6-phosphate dehydrogenase (G6PDH), a

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

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

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

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

90 h activities of NADP-dependent malic enzyme (NADP-ME), NAD-dependent malic enzyme (NAD-ME) and phosph

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

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

93 cting proteins, namely nitrite reductase, Fd:NADP+ oxidoreductase, and Fd:thioredoxin reductase.

94 nly the input of electrons from a ferredoxin NADP reductase (Pa Fpr), the release of iron stored in P

95 in the presence of P. aeruginosa ferredoxin NADP reductase (FPR) and NADPH, the heme in BfrB remains

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

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

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

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

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

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

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

103 2S] ferredoxin (PetF), reduced by ferredoxin-NADP(+) reductase (FNR) using NADPH, has been implicated

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

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

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

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

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

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

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

111 n kinetics in the presence of Fd, ferredoxin:NADP(+)-oxidoreductase (FNR), and NADP(+).

112 isoproteins of the photosynthetic ferredoxin:NADP(+) reductase (pFNRI and pFNRII).

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

114 y is observed when the flavodoxin/flavodoxin NADP(+) oxidoreductase/NADPH reducing system is used in

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

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

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

118 NADPH and not by NADH, suggesting a role for NADP(+) in the stabilization of intermediates in the rea

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

120 rom both NAD-ME, one PCK and two of the four NADP-ME genes were detectable in these veinal cells.

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

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

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

124 8-fold reversal of coenzyme selectivity from NADP(+) to NAD(+).

125 tinic acid moiety have been synthesized from NADP enzymatically using Aplysia californica ADP-ribosyl

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

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

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

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

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

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

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

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

134 The structures have NADP(H) and (hydroxy)ornithine bound in a solvent-expose

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

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

137 dopts a conformation that sterically hinders NADP(H) binding.

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

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

140 to malate valve capacity, with decreases in NADP-malate dehydrogenase activity (but not protein leve

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

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

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

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

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

146 Interestingly, NADP(+) and G6P also induced nuclear O(2)(.-) production

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

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

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

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

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

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

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

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

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

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

157 2',7'-dichlorofluorescein diacetate), NADPH, NADP(+) and ATP contents (spectrophotometry), matrix met

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

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

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

161 increases of the ATP concentration and NADPH/NADP(+) ratio in response to KIC were largely blunted in

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

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

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

165 ion activity under infection, the host NADPH/NADP ratio increased two-fold in infected cells.

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

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

168 ulted in a significant decrease in the NADPH:NADP(+) ratio during stimulation with glucose but not gl

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

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

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

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

173 umor cell death occurs through activation of NADP(+) oxidase and increased intracellular Ca(2+) level

174 mina, mid-veins possessed high activities of NADP-dependent malic enzyme (NADP-ME), NAD-dependent mal

175 The activity of NADP-malic enzyme and generation of reactive oxygen spec

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

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

178 ne with an alanine did not affect binding of NADP(+) but resulted in the enzyme lacking the ability t

179 Binding of NADP(+) is accompanied by the net release of approximate

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

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

182 well as reduced AfUGM after dissociation of NADP(+).

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

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

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

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

187 uses mitochondrial and cytosolic isoforms of NADP(+)/NADPH-dependent isocitrate dehydrogenase, and su

188 We measured tissue levels of NADP-linked isocitrate dehydrogenase (NADP-ICDH), glucos

189 Mutations of NADP(+)-dependent isocitrate dehydrogenases encoded by I

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

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

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

193 ion of NADPH is identical to the position of NADP(+) with the nicotinamide ring well ordered within t

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

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

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

197 ized by G6P dehydrogenase in the presence of NADP+, and the stoichiometrically generated NADPH is the

198 decarboxylation of malate in the presence of NADP.

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

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

201 bstrate probes was determined by the rate of NADP(+) formation and compared with fluorescent product

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

203 nd cofactor kinetics, following reduction of NADP(+) to NADPH.

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

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

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

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

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

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

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

211 The rotation of NADP(+) permits the substrate to gain access to the reac

212 ecreased by a factor of two, whereas that of NADP(+) remains the same.

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

214 relatively smaller effect of the mutation on NADP(+) binding.

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

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

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

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

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

220 31)-Asn(635) loop to a position that permits NADP(H) binding.

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

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

223 nicotinamide adenine dinucleotide phosphate (NADP(+)); the NADPH thereby generated reduces the tetraz

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

225 nicotinamide adenine dinucleotide phosphate (NADP) to NADPH.

226 eotide phosphate (NAADP) from NAD phosphate (NADP).

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

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

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

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

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

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

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

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

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

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

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

238 to alpha-ketoglutarate (alpha-KG) and reduce NADP to NADPH.

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

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

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

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

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

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

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

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

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

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

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

250 The recombinant protein exhibits robust NADP(+)-dependent CH(2)-THF dehydrogenase activity when

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

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

253 log is reduced by a glutaredoxin rather than NADP-thioredoxin reductase.

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

255 ural and biochemical evidence indicates that NADP(+) remains bound throughout the oxidative half-reac

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

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

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

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

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

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

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

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

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

265 In the NADP(+)-free structure, the loop adopts a conformation t

266 stress is associated with an increase in the NADP(+)/NADPH ratio and may result from a decrease in NA

267 ach subunit with a secondary mutation in the NADP/H binding site.

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

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

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

271 the heat capacity change for binding of the NADP(+) to the C298S.

272 Point mutations of the NADP(+)-dependent isocitrate dehydrogenases 1 and 2 (IDH

273 Monoallelic point mutations of the NADP(+)-dependent isocitrate dehydrogenases IDH1 and IDH

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

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

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

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

278 mic differences in the E:THF:NADPH and E:THF:NADP(+) product ternary complexes are difficult to ratio

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

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

281 c nuclei to generate O(2)(.-) in response to NADP(+) and G6P.

282 relating Glc-6-PD activity and the NADPH-to-NADP(+) ratio to the HPV response clearly indicated a po

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

284 exhibits strong cofactor selectivity toward NADP(H).

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

286 Recombinant DHCH1 showed typical NADP(+)-dependent methylene tetrahydrofolate DH and 5,10

287 te binding, while a proton was released upon NADP(+) binding.

288 N. crassa LAD that are capable of utilizing NADP(+) as cofactor, yielding the first example of LAD w

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

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

291 al structures of the mutant without and with NADP(+) revealed that the two flavin domains are joined

292 omparison of the structures without and with NADP(+) shows movement of the Gly(631)-Asn(635) loop.

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

294 ng that Af SidA forms a ternary complex with NADP(+) and l-ornithine during catalysis.

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

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

297 nd AKR4C9 (1.25 A) in ternary complexes with NADP(+) and acetate.

298 ld in Deltapos5 mitochondrial extracts, with NADP(+) diminished to a lesser degree.

299 The structure with NADP(+) shows movement of the Gly(631)-Asn(635) loop to

300 K) catalyzes phosphorylation of NAD to yield NADP.