ライフサイエンスコーパス: NADPH

1 NADPH is a critical reductant needed in cancer cells to

2 NADPH oxidase 1 (NOX1), a membrane-bound flavin dehydrog

3 NADPH oxidase 4 (NOX4) enzyme, which catalyzes the reduc

4 NADPH oxidase pathway modulators decreased ROS productio

5 NADPH oxidase-deficient (gp91(phox) knockout [KO]), iNOS

6 NADPH oxidase-derived excessive production of reactive o

7 NADPH oxidases (Noxes) produce ROS that regulate cell gr

8 NADPH oxidases (NOXs) are involved in inflammation, angi

9 NADPH oxidases (NOXs) are the only enzymes exclusively d

10 NADPH oxidases contribute to LPS-induced reactive oxygen

11 NADPH-cytochrome P450 reductase is a multi-domain redox

12 NADPH:protochlorophyllide oxidoreductase (POR) is a key

13 e generated by two oxidants, catechol/Cu(2+)/NADPH and Fenton's reagent, were located and compared.

14 most frequently oxidized by catechol/Cu(2+)/NADPH with relative oxidation of 5.6, 7.2, 2.6, and 10.7

15 Either loss of memo-1 or increasing BLI-3/NADPH oxidase activity by overexpression is sufficient t

16 an enhanced interaction of RHO-1 with BLI-3/NADPH oxidase, thereby stimulating ROS production that s

17 ty, MEMO-1, as a protein that inhibits BLI-3/NADPH oxidase.

18 In many tissues, type 4 NADPH oxidase is induced upon ischemia or hypoxia, conve

19 tes expression of Dual oxidase 1 (Duox-1), a NADPH oxidases known to generate H2O2.

20 2X7R agonist, BzATP, and was attenuated by a NADPH oxidase inhibitor apocynin.

21 thrine, a protein kinase C inhibitor, DPI, a NADPH-dependent oxidase (NOX) inhibitor, GKT137831, a NO

22 PpeS6PDH encodes a NADPH-dependent sorbitol-6-phosphate dehydrogenase, the

23 by pretreatment with diphenylene iodonium, a NADPH oxidase inhibitor.

24 nuous layer 2 modules are positive for AChE, NADPH-d, GAD, and CO throughout the rostrocaudal LCIC.

25 In addition, NADPH oxidase inhibitor diphenylene iodonium significant

26 lation of beta2-integrin-dependent adhesion, NADPH oxidase, and a subset of protein kinases.

27 Moreover, oxidative stress (ADP, NADPH, and Fe(3+)) resulted in the robust production of

28 ted as competitive inhibitors of UGM against NADPH with Ki values of 6 microM and 74 microM, respecti

29 thetic photosystem 1 complex, itself also an NADPH oxio-reductase.

30 rimary sequence that had been assigned as an NADPH-dependent thioredoxin reductase (NTR).

31 dehydrogenase-related protein Ayr1 forms an NADPH-regulated channel.

32 In addition, chloroplasts harbor an NADPH-dependent Trx reductase, which has a joint Trx dom

33 dehyde to their corresponding alcohols in an NADPH-dependent manner.

34 ehydrogenase RDH8 to all-trans-retinol in an NADPH-dependent reaction.

35 ining NADPH-dependent TrxRs (NTR), lacked an NADPH-binding site and was dependent on reduced coenzyme

36 Aryl amines also combine with Cu(2+) and NADPH to form reactive oxygen species (ROS) that oxidize

37 renal levels of Bax, cleaved caspase-3, and NADPH oxidase-4 expression and reactive oxygen species (

38 ed with an increase in F- actin assembly and NADPH oxidase activity.

39 f redox components (glutathione contents and NADPH-generating enzymes) prevents full priming of the s

40 t and protein expression of all the HIFs and NADPH oxidase 4 seen in PE compared to NT at sea level w

41 Metabolites can react with metal ions and NADPH to oxidize DNA or participate in SN2 reactions to

42 NADH-dependent SAM:C-methyltransferase, and NADPH-dependent CDP-3-C-methyl-6-deoxyhexose 4-reductase

43 ROS originate from mitochondria and NADPH oxidases.

44 d inflammasome activation, mitochondrial and NADPH-oxidase-dependent production of reactive oxygen sp

45 intermediate in this reaction, with NADH and NADPH (the reduced forms of nicotinamide adenine nucleot

46 tigations showed that the levels of NADH and NADPH diminish by up to approximately 50% within 24 h; c

47 important cofactors, such as ATP, NADH, and NADPH.

48 adenine dinucleotide phosphate (NADP(+) and NADPH), and adenosine triphosphate (ATP) and its precurs

49 adenine dinucleotide phosphate (NADP(+) and NADPH); coenzymes of energy including adenosine triphosp

50 (Delta/+) ECs and was suppressed by PI3K and NADPH oxidase 2 inhibitors.

51 yme-catalyzed H-D exchange between water and NADPH enables accurate interpretation of deuterium traci

52 yme-catalyzed H-D exchange between water and NADPH.

53 nucleotides, methionine, and the antioxidant NADPH.

54 pathways, thereby depleting the antioxidants NADPH and glutathione.

55 eoxy product when incubated with AprD4/AprD3/NADPH.

56 ires ROS generated by the defense-associated NADPH oxidase, RBOHD.

57 onally interacts with microtubule-associated NADPH oxidase (Nox) 2, and inhibition of Nox2 attenuated

58 on of the thylakoid proton motive force, ATP/NADPH balancing mechanisms (cyclic and noncyclic alterna

59 Because NADPH is required for processes that detoxify ROS, condi

60 The relationship between NADPH oxidase and HV 1 has become a paradigm that somewh

61 oduction in LSS, implicating a p47phox-bound NADPH oxidase (NOX) in mediating basal NO production.

62 Apoplastic ROS homeostasis controlled by NADPH oxidases as well as by secreted type III peroxidas

63 n reactive oxygen species (ROS) generated by NADPH oxidase, but Mtuberculosis fails to generate a rob

64 quired for Mtuberculosis to evade killing by NADPH oxidase and LAP.

65 re, we determine the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specif

66 d the amount of superoxide anion produced by NADPH oxidase was measured by spectrophotometry through

67 ipheral NKT cells were primarily produced by NADPH oxidases and not mitochondria.

68 Reactive oxygen species (ROS) produced by NADPH phagocyte oxidase isoform (NOX2) are critical for

69 sfer in comparison to enzyme regeneration by NADPH.

70 se cytochrome P450 BM3 that is restricted by NADPH dependence.

71 During catalysis, NADPH-derived electrons transfer into FAD and then distr

72 .92-7.38] mg/L; P<0.01) and endothelial cell NADPH oxidase expression (P<0.05).

73 c NAD(+) kinase levels and revealed cellular NADPH dynamics under oxidative stress depending on gluco

74 We demonstrate that the chloroplast NADPH dehydrogenase complex, a homolog to respiratory Co

75 h over expression of key enzymes in cofactor NADPH generating process for NADPH pool.

76 becomes accessible when the reduced cofactor NADPH is bound, involves transient sampling of a higher

77 A linear arrangement of cofactors (NADPH, FAD, and two membrane-embedded heme moieties) inj

78 gulatory roles contain additional cofactors, NADPH and two phosphopantetheine molecules, which are sh

79 y related NO synthases (NOSs), which contain NADPH/FAD- and FMN-binding domains.

80 on structure of a ternary complex containing NADPH and a P5C/proline analog provides a model of the M

81 gh structurally similar to flavin-containing NADPH-dependent TrxRs (NTR), lacked an NADPH-binding sit

82 which, in turn, activates a Nox2-containing NADPH oxidase, leading to cerebrovascular oxidative stre

83 Chemokine-controlled NADPH oxidases and metabolically controlled mitochondria

84 nt IDH2 did not display isocitrate-dependent NADPH production above vector control levels, in contras

85 int specifically regulates septin-dependent, NADPH oxidase-regulated F-actin dynamics to organize the

86 e adenine dinucleotide phosphate-diaphorase (NADPH-d), glutamic acid decarboxylase (GAD), cytochrome

87 ochondrial malic enzymes revealed diminished NADPH production and consequent high levels of reactive

88 in, and hindlimb that only in the brain does NADPH oxidase 4 (NOX4) lead to ischemic damage.

89 e reactive oxygen species-generating enzyme, NADPH oxidase 4 (Nox4), regulates a number of physiologi

90 solic component of the ROS producing enzyme, NADPH oxidase, and the increase in amounts of phosphoryl

91 brafish larvae, activation of the epithelial NADPH oxidase Duox at the wound margin is required early

92 Activation of Schwann cell TRPA1 evoked NADPH oxidase 1 (NOX1)-dependent H2O2 release, and silen

93 To date, studies examining NADPH production with deuterated carbon sources have fai

94 Mutants of the root-expressed NADPH oxidase RBOH C, but not rbohD, showed enhanced hyd

95 and characterization of a thermostable F420: NADPH oxidoreductase (Tfu-FNO) from T. fusca, the first

96 s, likely affecting the pools of ferredoxin, NADPH and NADH, as well as influencing metabolic pathway

97 of endogenous phosphatase activity following NADPH oxidase (NOX) inhibition.

98 of malate to pyruvate and are essential for NADPH regeneration and reactive oxygen species homeostas

99 netically encoded fluorescent indicators for NADPH (iNap sensors) with various affinities and wide dy

100 mes in cofactor NADPH generating process for NADPH pool.

101 had higher levels of Rac1-GTP, required for NADPH oxidase activation, than sham control kidneys, and

102 arge conformational changes are required for NADPH to reduce the FAD.

103 reviously demonstrated an important role for NADPH oxidase (NOX)-derived superoxide production during

104 Glucose released from glycogen and used for NADPH/glutathione reduction renders nematodes and human

105 ased the generation of superoxide anion from NADPH oxidase, as well as the amount of hydrogen peroxid

106 tion of reactive oxygen species derived from NADPH oxidase (NOX)-4 and mitochondrial sources.

107 tem and reactive oxygen species derived from NADPH oxidase (Nox).

108 Plant P450s receive electrons from NADPH P450 oxidoreductase (POR) to orchestrate the bio-s

109 confirming that the current originates from NADPH oxidase activity.

110 ductase required for electron transport from NADPH to cytochrome P450.

111 at the regulatory cues conformationally gate NADPH-binding, implicitly providing a handle for activat

112 This generates NADPH in the mitochondria, enabling cells to mitigate mi

113 that the reactive oxygen species-generating NADPH oxidase-4 (Nox4) is induced downstream of ATF4, bi

114 ar distribution of the superoxide generating NADPH oxidase (NOX) in AVP-expressing hypothalamic parav

115 mannan-induced arthritis in SKG mice and how NADPH oxidase 2-derived reactive oxygen species (ROS) re

116 Human NADPH-cytochrome P450 oxidoreductase (POR) gene mutation

117 Moreover, CpsA was sufficient to impair NADPH oxidase recruitment to fungal particles that are n

118 enzyme deficiency, which results in impaired NADPH production, provides a prime 'collateral lethality

119 Previous studies implicate NADPH oxidase (Nox) proteins as important reactive oxyge

120 alterations and also reverted the changes in NADPH oxidase expression triggered by Ang II.

121 cells exquisitely sensitive to decreases in NADPH concentration.

122 ilarly, neutrophils with a genetic defect in NADPH oxidase fail to induce either actin and tubulin po

123 was partially restored in mice deficient in NADPH oxidase, Atg5, or Atg7, demonstrating that CpsA ma

124 Six genes encoding the key enzymes in NADPH generation were over-expressed in the gamma-PGA pr

125 FNR, the top hit enabled a 60 % increase in NADPH-driven H2 production rates.

126 nthesis pathway and one carbon metabolism in NADPH production and the maintenance of redox homeostasi

127 )-producing systems in vascular wall include NADPH (reduced form of nicotinamide adenine dinucleotide

128 a marked increase in antioxidants including NADPH and reduced glutathione.

129 ing of carbohydrate metabolism and increased NADPH levels in a pentose phosphate pathway (PPP)-depend

130 High-glucose increases NADPH oxidase 4 (NOX4) expression, reactive oxygen speci

131 ect of LC on angiotensin II (Ang II)-induced NADPH oxidase activation in NRK-52E cells.

132 horbol 12-myristate 13-acetate (PMA)-induced NADPH oxidase activity were increased in RacET and corre

133 olite profiling discovered that insufficient NADPH due to GLS2 underexpression was responsible for th

134 revealed that HDM-induced cellular injury is NADPH oxidase (NOX)-dependent, and apocynin, a NOX inhib

135 Though isolated NADPH does not undergo H-D exchange with water, such exc

136 h a signaling pathway requiring Src kinases, NADPH oxidase, superoxide radical anion, and hydrogen pe

137 with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity an

138 More recently, a plastid-localized NADPH-dependent Trx reductase (NTR) with a joint Trx dom

139 cluding Toll-like receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation.

140 f reactive chemical species by mitochondria, NADPH oxidase, and type 2 nitric-oxide synthase (NOS-2)

141 uantification of cytosolic and mitochondrial NADPH pools that are controlled by cytosolic NAD(+) kina

142 o-oxidative response to Ang II by modulating NADPH oxidase enzyme via reducing the activity of PKC an

143 Moreover, using the iNap sensors we monitor NADPH fluctuations during the activation of macrophage c

144 ensors will be valuable tools for monitoring NADPH dynamics in live cells and gaining new insights in

145 ditions PntAB functions to balance the NADH: NADPH equilibrium specifically in the direction of NADPH

146 se was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll

147 on of recombinant GM-CSF enhanced neutrophil NADPH oxidase function, conidiacidal activity, and lung

148 a strategy to inhibit assembly of neutrophil NADPH oxidase.

149 ectin-3-induced activation of the neutrophil NADPH oxidase was abrogated by bacterium-derived proteol

150 ely because enzymes of the primary nighttime NADPH-producing pathway are direct targets of RpaA.

151 ine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

152 ine, which was normalized by a specific Nox2 NADPH oxidase inhibitor.

153 ase B was increased in hIRECO EC as was Nox2 NADPH oxidase-dependent generation of superoxide, wherea

154 f reactive oxygen species (ROS) via the NOX3 NADPH oxidase pathway in the cochlea.

155 esponse initiated by ROS generation via NOX3 NADPH oxidase, leading to inhibition of STAT1.

156 mational changes, contribute to the observed NADPH-dependent shift in Kd.

157 xidative pentose phosphate pathway to obtain NADPH.

158 eripheral membrane protein in the absence of NADPH and will transition to an integral membrane protei

159 ibutes to the production and accumulation of NADPH to levels that are sufficient to combat oxidative

160 n species in the heart through activation of NADPH oxidase 2 (NOX2).

161 en peroxide resulting from the activation of NADPH oxidase 4 (NOX4).

162 lly, CD47 blockade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phago

163 in the presence of stoichiometric amounts of NADPH or greater.

164 -phosphogluconolactonase, a key component of NADPH synthesis, potently synergizes MB activity.

165 re Nox2 and p67phox, which are components of NADPH oxidase, compared to triceps surae muscles of 'fre

166 alpha-ketoglutarate-dependent consumption of NADPH compared to wild-type IDH2 or vector control.

167 We identified deficiency of NADPH oxidase 2 (NOX2) as the molecular underpinning of

168 antioxidant functions; however, detection of NADPH metabolism in living cells remains technically cha

169 equilibrium specifically in the direction of NADPH.

170 two electrons delivered by the FMN domain of NADPH-cytochrome P450 reductase.

171 vivo as an F420 reductase at the expense of NADPH, similar to its counterpart in Streptomyces griseu

172 cular endothelial cell protein expression of NADPH oxidase.

173 Within the family of NADPH oxidases, NOX4 is unique as it is predominantly lo

174 gree of partitioning of CPR as a function of NADPH concentration.

175 s have failed to account for roughly half of NADPH's redox active hydrogen.

176 s, and rapid NET formation is independent of NADPH oxidase activity.

177 c organisms, and pharmacologic inhibition of NADPH-oxidase partially impairs NET production.

178 L. amazonensis is impaired by inhibitors of NADPH oxidase, Syk, focal adhesion kinase, and proline-r

179 f data about the role of the Nox5 isoform of NADPH oxidase in animal models of diabetic nephropathy s

180 ion of FST decreased the expression level of NADPH oxidase 1 (NOX1) and NOX5 as well as the productio

181 was also associated with increased levels of NADPH reflecting a higher activation of pentose phosphat

182 DH1 silencing in GBM cells reduced levels of NADPH, deoxynucleotides, and glutathione and increased t

183 has been associated with the maintenance of NADPH oxidase activity and the generation of reactive ox

184 MP and ammonia with concomitant oxidation of NADPH.

185 a/beta leading to reduced phosphorylation of NADPH oxidase components p47 (phox) and p40 (phox) in co

186 burst caused by decreased phosphorylation of NADPH oxidase cytosolic components that are augmented by

187 se flux, correcting imbalanced production of NADPH and NADH, were enabled by direct mutations to the

188 by generating ATP without net production of NADPH.

189 reduced glutathione, but also on the rate of NADPH production, contradicting the conclusions of some

190 In the present work, we examined the role of NADPH oxidase 4 (Nox4) in LPS-induced TLR4 responses in

191 ore, this study aimed to analyze the role of NADPH oxidase and inducible nitric oxide synthase (iNOS)

192 pentose phosphate pathway is a major site of NADPH production in the cell, which is used to maintain

193 accurate assessment of biological sources of NADPH's high energy electrons.

194 etinol to retinaldehyde, and two subunits of NADPH-dependent dehydrogenase reductase 3 (DHRS3), which

195 n hippocampal neurons via diverse effects on NADPH oxidase activity and dendritic spine morphology.

196 r cells is to target their heavy reliance on NADPH.

197 educed Atox1 target proteins such as p47phox NADPH oxidase and cyclin D1 as well as extracellular mat

198 r concentrations of NAD(P)H and particularly NADPH.

199 of the enzyme reduction by the redox partner NADPH-cytochrome P450 oxidoreductase, and the amount of

200 oding the p47(phox) subunit of the phagocyte NADPH oxidase (NOX2), as the putative underlying causal

201 y has now extended well beyond the phagocyte NADPH oxidase - an industrial strength producer of react

202 cy marked by a defect in NOX2, the phagocyte NADPH oxidase.

203 hich is required to stimulate the phagocytic NADPH-oxidase that generates reactive oxygen species.

204 nicotinamide adenine dinucleotide phosphate (NADPH) in p53-deficient cancer cells.

205 nicotinamide adenine dinucleotide phosphate (NADPH) is essential for biosynthetic reactions and antio

206 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation because pretreatment of eosino

207 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (NOX-2) expression.

208 Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce ROS locally in response to vario

209 nicotinamide adenine dinucleotide phosphate (NADPH) production and imbalanced redox homeostasis in er

210 nicotinamide adenine dinucleotide phosphate/NADPH levels, phagocytic reactive oxygen species product

211 biosynthesis of glutathione, phospholipids, NADPH, and coenzyme Q10.

212 a strong tendency to maintain physiological NADPH homeostasis, which is regulated by glucose-6-phosp

213 , response to sulfur starvation, potentially NADPH-producing pathways involving (S)-malate and ornith

214 NADH into the lipid biosynthetic precursors NADPH or acetyl-CoA.

215 aining the cellular redox balance, producing NADPH for biosynthesis by recycling the two other primar

216 crease mitochondrial antioxidant production (NADPH and glutathione).

217 rived macrophages (MDMs) for ROS production, NADPH assembly capacity, protein kinase C expression, an

218 3 could increase the two major PPP products, NADPH and nucleotides, only nucleotide production was es

219 es containing the DeltacpsA mutant recruited NADPH oxidase, produced ROS, associated with LC3, and ma

220 In these 3 brothers strongly reduced NADPH oxidase function was found in granulocytes, leadin

221 utathione synthetase, glutathione reductase, NADPH-cytochrome P450 reductase, biliverdin reductase, a

222 s through the mycothiol/mycothione reductase/NADPH pathway to activate TP053, preferentially via a di

223 nsatory mechanisms that include up-regulated NADPH production via the pentose phosphate pathway as we

224 The family prototype PDIA1 regulates NADPH oxidase signaling and cytoskeleton organization, h

225 The expression level of GLS2 and related NADPH production capacity is associated with the regiona

226 thermore, IL-12-mediated protection required NADPH oxidase activity.

227 reduction in non-native disulfides requires NADPH as the ultimate electron donor, and a robust cytos

228 SHP2 oxidation requires NADPH oxidases (NOXs), and oxidized SHP2 co-localizes wi

229 We see NADPH bound to the Rossmann fold, over 25 A from the pre

230 These cells with their seven NADPH oxidase (NOX) isoforms provide a vast realm of mec

231 ntial gene expression in JAK-STAT signaling, NADPH oxidation, and other cancer-related pathways.

232 nase 2 (COX2))- and reactive oxygen species (NADPH oxidase 4 (NOX4))-generating enzymes by classical

233 reactive oxygen species derive from specific NADPH oxidase isoforms remains ill defined.

234 vax malaria, patients with a normal standard NADPH fluorescent spot test result ( greater, similar30%

235 that the Leishmania GMPR catalyzed a strict NADPH-dependent reductive deamination of GMP to produce

236 ght using the relatively oxidizing substrate NADPH, whereas the canonical ferredoxin-thioredoxin syst

237 on of reduced glutathione (GSH) by supplying NADPH to glutathione reductase or thioredoxin reductase.

238 oxide dismutase and catalase, and suppressed NADPH oxidase and reactive oxygen species (ROS) producti

239 Double-labeling experiments confirm that NADPH-d, the most consistent developmental modular marke

240 Together, these findings demonstrate that NADPH oxidase-induced redox signaling initiates a transc

241 ollectively, these results demonstrated that NADPH generation via over-expression of Zwf is as an eff

242 We also found that NADPH- and xanthine oxidase-dependent reactive oxygen sp

243 n-pumping stoichiometry, we hypothesize that NADPH dehydrogenase not only efficiently contributes to

244 Our results indicate that NADPH oxidase is important to control A. actinomycetemco

245 We conclude that this study shows that NADPH deficiency protects mice from developing OXPHOS dy

246 The NADPH oxidase (NOX) isoform NOX4 has been linked with di

247 ots with the ROS scavenger ascorbate and the NADPH oxidase inhibitor diphenyliodonium and analysis of

248 ar loops on the transmembrane domain and the NADPH-oxidizing dehydrogenase domain.

249 ) exposure and intrinsic factors such as the NADPH oxidases produce high levels of reactive oxygen sp

250 Arg-1229) forming a salt bridge between the NADPH/FAD and FMN domains in the conformationally closed

251 ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex.

252 of toxic reactive oxygen metabolites by the NADPH oxidase and myeloperoxidase.

253 ctive oxygen species (ROSs) generated by the NADPH oxidase Duox in epithelial disc cells.

254 strate for FosDH2, was shown to catalyze the NADPH-dependent stereospecific reduction of 3-ketobutyry

255 CBR1 catalyzes the NADPH- dependent production of 20beta-dihydrocortisol (2

256 strongly depend on activation of either the NADPH oxidase DUOX1 or the homolog NOX2, depending on th

257 activity in periodic samples taken from the NADPH-driven reaction solutions.

258 Furthermore, the NADPH oxidase NOX4 inhibits this transition and therefor

259 tional freedom impact the following: (i) the NADPH interaction; (ii) kinetics of electron loading (fl

260 disease patients, carrying mutations in the NADPH oxidase complex or a MPO-deficient patient were ex

261 taining membrane proteins, which include the NADPH oxidase proteins (NOX/DUOX).

262 28-fold, which led to the improvement of the NADPH generation, and decrease of accumulation of by-pro

263 TRAF3 is central in the activation of the NADPH oxidase (Nox)-2 component p40phox and the elevatio

264 s to this defect in terms of assembly of the NADPH oxidase complex and subsequent ROS production.

265 ng to p47(phox), a critical component of the NADPH oxidase complex, disrupting the complex and facili

266 ed expression of cytosolic components of the NADPH oxidase complex.

267 nd p38 that are required for assembly of the NADPH oxidase complex.

268 Eros is required for expression of the NADPH oxidase components, gp91phox and p22phox Consequen

269 1, followed by direct phosphorylation of the NADPH oxidase RBOHD, resulting in elevated production of

270 a toggle switch, which affects access of the NADPH substrate to the enzyme.

271 During development of the NADPH-driven assay and while characterizing the Clostrid

272 ore generated a conditional knock-out of the NADPH-P450 oxidoreductase (Por) gene combined with Il2rg

273 t many also can catalyze a new reaction, the NADPH-dependent reduction of alphaKG to d-2-hydroxygluta

274 nicotinamide ring into the active site, the NADPH cofactor remodels the enzyme structure and the con

275 discover inhibitors of UGM by targeting the NADPH binding site using an ADP-TAMRA probe in a high-th

276 far been only observed in patients with the NADPH oxidase deficiency chronic granulomatous disease,

277 Consistently, PLC2 associates with the NADPH oxidase RBOHD, suggesting its potential regulation

278 we identify an ATP-binding motif within the NADPH oxidase isoform, NOX4, and show that ATP directly

279 Stimulated neutrophils activate their NADPH oxidase (NOX2) to generate large amounts of supero

280 In the excited state of the E:THF:NADPH product release complex, the reduced nicotinamide

281 ance of the redox balance by contributing to NADPH production through the reaction catalyzed by methy

282 bution to the resistance of Mtuberculosis to NADPH oxidase and LC3 trafficking in vivo.

283 e dehydrogenase 2 (IDH2) converts NADP(+) to NADPH and promotes regeneration of reduced glutathione (

284 activity underlie conidial susceptibility to NADPH (reduced form of nicotinamide adenine dinucleotide

285 hough CF MDMs generally have increased total NADPH component protein expression, they demonstrate dec

286 hibited about ~6-fold lower affinity towards NADPH than wtDHFR.

287 H2O2 Intriguingly, we discovered that TrxR1/NADPH directly protects PTP1B from inactivation when pre

288 is subsequently converted into preQ1 in two NADPH-dependent reduction steps.

289 genase IDH1 is the most strongly upregulated NADPH-producing enzyme in glioblastoma (GBM).

290 droxycinnamoyl-coenzyme A (CoA) esters using NADPH to produce hydroxycinnamyl aldehyde precursors in

291 tochrome P450-reductase (CPR) is a versatile NADPH-dependent electron donor located in the cytoplasmi

292 article, we demonstrate that ROS induced via NADPH oxidase during the early stages of L. amazonensis

293 stimulated NET release may arise in part via NADPH oxidase-independent mechanisms.

294 We show D2O labels fatty acids primarily via NADPH.

295 ion increased endothelial ROS production via NADPH oxidase signaling, up-regulated Nox4 expression, a

296 vation generates reactive oxygen species via NADPH oxidase, reducing the palmitoylation of receptor-a

297 d to the intrinsic pathway that obtains when NADPH is absent.

298 is by forming stably functional complex with NADPH oxidase 2 (Nox2).

299 Structures of binary complexes of PYCR1 with NADPH or proline determined at 1.9 A resolution provide

300 lavin reduction is achieved by reaction with NADPH.