ライフサイエンスコーパス: NADPH

1 NADPH diaphorase is used as a histochemical marker of ni

2 NADPH facilitates glucose-stimulated insulin secretion (

3 NADPH oxidase 4 (NOX4) is the most abundant NOX isoform

4 NADPH oxidase inhibition did not prevent cross-talk inhi

5 NADPH-thioredoxin reductase C (NTRC) forms a separate th

6 1 knockdown resulted in high Rac1 and Nox 1 (NADPH oxidase 1) activity, increased ROS (oxidative stre

7 ite Cys peptides of glutathione reductase 2, NADPH-thioredoxin reductase a/b, and thioredoxin-o1 show

8 Here, we identified type 5 NADPH oxidase (NOX5), a calcium-activated, ROS-forming e

9 e P450 (heme-binding) catalytic domain and a NADPH-cytochrome P450 reductase (CPR) domain containing

10 n by acetaldehyde in these cells initiates a NADPH oxidase-1-dependent (NOX1-dependent) production of

11 nce of acetyl-CoA, UDP- N-acetylglucosamine, NADPH, and ATP, we have developed a system capable of sy

12 Activated NADPH oxidase generates reactive oxygen species and elev

13 shows that the RIPK3-MLKL pathway activates NADPH oxidase but requires, in addition to p38 MAPK and

14 iols to solutions of NBT plus beta- or alpha-NADPH elicited rapid formation of diformazan in the abse

15 ddition of S-nitrosothiols or beta- or alpha-NADPH to solutions of NBT did not elicit diformazan, (3)

16 An NADPH oxidase assay proved that the inhibitory effect of

17 iome was associated with increased NOX-2, an NADPH oxidase isoform.

18 ME), a superoxide scavenger (Tempol), and an NADPH oxidase inhibitor (apocynin), as well as during pe

19 In addition, chloroplasts contain an NADPH-dependent redox system, termed NTRC, which allows

20 DUOX1, an NADPH oxidase family member, catalyzes the production of

21 downstream gene called arsH that encodes an NADPH-dependent flavin mononucleotide reductase.

22 MMe macrophages release IL-6 in an NADPH oxidase 2 (NOX2)-dependent manner, which signals t

23 te gene hits, TraesCS4D02G352200 (TaNox8; an NADPH oxidase) and TraesCS4D02G350300 (a rhomboid-like p

24 e find that RAC2(E62K) retains binding to an NADPH oxidase (NOX2) subunit, p67(phox), and to the RAC-

25 1 GAS can be cleared by neutrophils using an NADPH oxidase-dependent mechanism in the lung.

26 NO to NO(3) (-) in the presence of O(2) and NADPH; however, NOS(g) did not protect Escherichia coli

27 ucose-6-phosphate dehydrogenase activity and NADPH levels were increased in SIRT6-overexpressing cell

28 ation of p38, JNK, caspase 3/7 activity, and NADPH oxidase 4 expression induced by high glucose level

29 beta1 trafficking that translocates aPLs and NADPH oxidase to the endosome.

30 ns as a dimer and produces NO from l-Arg and NADPH in a tetrahydrobiopterin (H(4)B)-dependent manner

31 ascade downstream of AMPK, affecting ATP and NADPH levels, glucose uptake, and reactive oxygen specie

32 etic organisms balance the levels of ATP and NADPH necessary for efficient photosynthesis(1,2).

33 nor additional demand for cofactors (ATP and NADPH).

34 impaired PR disturbs the balance of ATP and NADPH, leading to the accumulation of H(2) O(2) that act

35 e mitochondrial electron transport chain and NADPH oxidase, respectively.

36 ression of TLR4, dual oxidase 2 (DUOX2), and NADPH oxidase 1 (NOX1).

37 expression of FOXO transcription factors and NADPH oxidase 4 (Nox4), a key regulator of reactive oxyg

38 features two domains for binding of FAD and NADPH, representative of class B flavin monooxygenases.

39 nd an intermediate adduct of finasteride and NADPH as NADP-dihydrofinasteride in a largely enclosed b

40 lity, restricted ribose/deoxyribose flow and NADPH production, an accumulation of alpha-ketoglutarate

41 xide synthase (NOS) immunohistochemistry and NADPH-diaphorase (NADPH-d) histochemistry, which yielded

42 Sso-KARI complexes, with NADH+inhibitor and NADPH+inhibitor at pH 7.5, which indicate that the bispe

43 (AMPK), Akt and eNOS, and inhibits iNOS and NADPH oxidase isoform 4 (NOX4), all of which are associa

44 ERK1/2 phosphorylation, internalization, and NADPH oxidase activity, yet lack of beta-arrestin recrui

45 ation of ERK, phosphoinositide 3-kinase, and NADPH oxidase-mediated reactive oxygen species generatio

46 ds on OmpU translocation to mitochondria and NADPH oxidase-mediated ROS production is due to activati

47 RIPK3), mixed lineage kinase-like (MLKL) and NADPH oxidase.

48 ys germination through the action of MPO and NADPH oxidase, and restricts fungal growth through NET r

49 rts the dinucleotide NADP(+) into NAD(+) and NADPH into NADH.

50 so accepted by human FMO1, and both NADH and NADPH cofactors could act as electron donors, a feature

51 Altering NADH and NADPH metabolism using drug strategies and IDH1 mutation

52 lly fluorescent metabolic cofactors NADH and NADPH with subcellular spatial resolution.

53 in being a dodecamer, bispecific to NADH and NADPH, and losing activity above pH 7.8.

54 tial roles in influencing levels of NADH and NADPH, in all analyzed organs of conventional mice.

55 thway induces acute synthesis of NADP(+) and NADPH.

56 n protein constructed of cytochrome P450 and NADPH-cytochrome P450 reductase domains.

57 p38 MAPK activation but proximal to PI3K and NADPH oxidase activation.

58 IV form a complex in the presence of PMB and NADPH, presumably to hand over the unstable MtmOIV produ

59 ted with fluxes through NADP(+)-reducing and NADPH-balancing reactions.

60 ficantly porous and exposed active site, and NADPH adopting a new conformation with the 2'-phosphate

61 ts signaling domain, which activates SYK and NADPH oxidase to cause phagosomal damage even when splic

62 ities of inducible nitric oxide synthase and NADPH oxidase 1 enzymes at myoendothelial projections in

63 phosphate pathway as a source of antioxidant NADPH, and maintenance of a high ratio of reduced to oxi

64 nd an enhanced abundance of the antioxidant, NADPH.

65 Activated neutrophils assemble NADPH oxidase to convert substantial amounts of molecula

66 with cofactor regenerating systems for ATP, NADPH, and amine donor, we established a one-pot enzyme

67 transforming growth factor beta (TGF-beta), NADPH oxidase isoform 4 (Nox4), caspase-3 and Bax.

68 tioselective cycloaddition as a bifunctional NADPH-dependent reductase/Diels-Alderase.

69 eduction cascade in plastids, combining both NADPH-thioredoxin reductase and thioredoxin activities o

70 equent reduction to l-cysteine depleted both NADPH and GSH pools, thereby allowing toxic accumulation

71 These defects were associated with both NADPH availability and ROS accumulation, suggesting that

72 or inhibitors that alter the ratio of bound NADPH to NADP(+) (and hence the record of sleep debt or

73 led that reduction of the flavin cofactor by NADPH is boosted by hispidin binding by nearly 100-fold.

74 reactive oxygen species (ROS) generation by NADPH oxidase complex and mitochondrial ROS.

75 This degradation is mediated by NADPH oxidase that produces highly oxidizing reactive ox

76 off-target oxygen free radicals produced by NADPH oxidase-1 (Nox1)(3,6) that otherwise elicited ER s

77 ROS produced by NADPH oxidases (Noxes), such as Nox2, are key components

78 sulting from the Grx reaction was reduced by NADPH and GSH reductase and this enzyme was essential be

79 ng-wavelength band when AsFMO was reduced by NADPH, probably representing the formation of a charge-t

80 h levels of reactive oxygen species (ROS) by NADPH oxidase that are crucial for host defense but can

81 wn from redox buffering circuits supplied by NADPH, and that the rate of electron flux through redox

82 is reduced to H(2)O by electrons supplied by NADPH.

83 encies is decreased mitochondrial one-carbon NADPH production that is associated with increased infla

84 lfite (SO(3)(2-)), and depletion of cellular NADPH.

85 presents a significant drain on the cellular NADPH pool and renders such cells dependent on the pento

86 structurally and quantitatively characterize NADPH oxidase in live cells.

87 Bsp5 in complex with d-arginine and coenzyme NADPH.

88 ied that IP4 competes with the NOX4 cofactor NADPH for binding and consequently inhibits NOX4.

89 means of a catalytic amount of the cofactor NADPH as hydride source as well as glucose as the reduci

90 way (PPP) inhibition depends on compensatory NADPH production through the mitochondrial one-carbon me

91 ively regulates the abundance of a conserved NADPH oxidase.

92 hox) to the membrane, resulting in decreased NADPH oxidase activity.

93 , a small-molecule PCNA inhibitor, decreased NADPH oxidase activation in vitro.

94 equired as the substrate of Ca(2+)-dependent NADPH oxidases, which catalyze a reactive oxygen species

95 ocks the generation of ROS by Rac1-dependent NADPH oxidases.

96 sustains both ATP levels and ROS-detoxifying NADPH.

97 ) immunohistochemistry and NADPH-diaphorase (NADPH-d) histochemistry, which yielded almost identical

98 Using different NADPH oxidase-deficient mice, we show that TSPO is a key

99 ely alleviated, suggesting that dysregulated NADPH oxidase activity is a key factor promoting autoinf

100 itol metabolism yields a "surplus" of either NADPH or NADH.

101 nce of excess H(2)O(2) and during enzymatic (NADPH/thioredoxin reductase/thioredoxin) and chemical (D

102 active oxygen species (ROS)-producing enzyme NADPH oxidase-4 (Nox4) in the pathogenesis of DPN.

103 rough inhibition of a ROS-generating enzyme, NADPH oxidase 4 (NOX4), which promotes cisplatin-resista

104 ge was absent in mice that lacked epithelial NADPH oxidase 1 (NOX1) activity.

105 The epithelial NADPH oxidase NOX1 is the primary source of luminal H(2)

106 Furthermore, excess NADPH, GTP and ADP greatly diminish N-malonylation near

107 BPSS2242 exhibited NADPH-dependent reductase activity toward diacetyl and m

108 work suggests a role for stromally expressed NADPH oxidase 4 (NOX4) as a modulator of reactive oxygen

109 ALR2 has three levels of affinity, first for NADPH, second for vitamin K1 and third for the substrate

110 l and preoptic nerve fibers labeled only for NADPH-d.

111 NADP(+) and therefore activates the PPP for NADPH and ribose-5-phosphate, which consequently detoxif

112 aining monooxygenase having a preference for NADPH.

113 ascular endothelial cells known to stain for NADPH diaphorase were rich in S-nitrosothiols, and (7) p

114 nd reduced NADH and its phosphorylated form, NADPH (NAD(P)H; 2.77 +/- 0.26 ns compared to 2.57 +/- 0.

115 Indeed, ROS forming NADPH oxidase (Nox) genes associate with hypertension, y

116 edicine, and reactive oxygen species forming NADPH oxidase type 4 (Nox4) as a primary causal therapeu

117 We found NADPH oxidase isoform 4 (NOX4) to be the main producer o

118 The enzyme receives two electrons from NADPH via thioredoxin reductase (TrxR) and passes them o

119 ses to change their cofactor preference from NADPH towards NADH and demonstrated their functionality

120 nally regulated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower incl

121 ssion, altered calcium release dynamics, how NADPH oxidase 2 is activated by and responds to stretch,

122 te reductase activity while showing improved NADPH-dependent activity.

123 Genetic defects in NADPH oxidase result in chronic granulomatous disease (C

124 A significant difference in NADPH was seen between cervical tumor orthotopic implant

125 However, increases in NADPH oxidase 1 (Nox1) mRNA expression were observed in

126 Tyr162 and Lys166 are involved in NADPH binding and mutation of Lys166 causes a conformati

127 , probably led to a significant reduction in NADPH-protochlorophyllide oxidoreductase in the yellow s

128 A reduction in NADPH-protochlorophyllide oxidoreductase, along with pho

129 oxidase subunit p47(phox), which results in NADPH oxidase activation.

130 more than 40 enzymes, prominently including NADPH oxidases and the mitochondrial electron transport

131 enal protein adducts together with increased NADPH (nicotinamide adenine dinucleotide phosphateoxidas

132 ells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the

133 ioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP).

134 ated acetylation of K337 strongly influences NADPH generation, lipid metabolism, and the susceptibili

135 In conclusion, metformin inhibited NADPH oxidase, which in turn suppressed ROS production a

136 PPE2 inhibited NADPH oxidase-mediated ROS generation in RAW 264.7 macro

137 ther, this study suggests that PPE2 inhibits NADPH oxidase-mediated ROS production to favor M. tuberc

138 However, STEAP1 lacks an intracellular NADPH-binding domain and does not exhibit cellular ferri

139 nd redox regulation, including intracellular NADPH oxidase-mediated ROS signalling.

140 I) reduction when fused to the intracellular NADPH-binding domain of its family member STEAP4, sugges

141 osed for induced oxidative stress, involving NADPH oxidase activation.

142 Reduction of oxidized RBD1 is NADPH dependent and can be mediated by ferredoxin-NADP(+

143 ded on mitochondrial ferredoxin FDX2 and its NADPH-coupled reductase FDXR.

144 tor of oxidative stress response through its NADPH 2' phosphatase activity.

145 ion from murine tissues dramatically lowered NADPH-dependent GSNOR activity.

146 nce of the oxidative pentose pathway, a main NADPH production route.

147 ve oxygen species production and maintaining NADPH levels.

148 ydrogenase (G6PD) is critical in maintaining NADPH, which is an important cofactor for the antioxidan

149 oduction contributes to inflammation, making NADPH oxidase a major drug target.

150 s in the oxidative PPP potentially maximizes NADPH reduction to counteract chemotherapy-induced react

151 e DUOX1-DUOXA1 interaction, a lipid-mediated NADPH-binding pocket and the electron transfer path.

152 gen species via the activation of membranous NADPH oxidase (from 15 min) and mitochondria (from 6 h)

153 ss caused by diamide (a drainer of metabolic NADPH) in the absence of any arsenic.

154 tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transc

155 inistration is mediated in part by microglia NADPH oxidase activation, and this is alleviated by the

156 ctive CI-dependent decrease in mitochondrial NADPH production pathway or genetic ablation of SHMT2 ca

157 folds, and PtmO8 and PtmO1, a pair of NAD(+)/NADPH-dependent dehydrogenases, subsequently work in con

158 by biosensors that detect pH, NAD(+), NADH, NADPH, histidine, and glutathione redox potential.

159 old motifs that bind the ADP moiety of NADH, NADPH, FADH and ATP.

160 ue to its ability to regenerate ATP and NADH/NADPH.

161 Leukocyte reduced NADP (NADPH) oxidase plays a key role in host defense and immu

162 with redox coenzymes (NAD(+), NADH, NADP(+), NADPH), energy coenzymes (ATP, ADP, AMP), antioxidants (

163 NAD/NADP was replaced by NADP/NADPH.

164 were not detected, pDCs regulated neutrophil NADPH oxidase activity and conidial killing.

165 angstrom crystal structure of the human NOCT*NADPH complex, which revealed that NOCT recognizes the c

166 We found that saturated fat activates NOX (NADPH oxidase), whereas polyunsaturated fat does not.

167 oxygen species generation by neutrophil NOX2 NADPH oxidase.

168 Inactivation of NOX2 NADPH oxidase in Pstpip2(cmo) mice did not affect IL-1be

169 The NOX2 NADPH oxidase (NOX2) produces reactive oxygen species to

170 pressure, glucose, F(2)-isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were measur

171 hydrogenase 2 was reduced, whereas the NOX2 (NADPH [nicotinamide adenine dinucleotide phosphatase] ox

172 de phosphatase] oxidase subunit 2) and NOX4 (NADPH [nicotinamide adenine dinucleotide phosphatase] ox

173 idase (NOX)4 promoter and induction of NOX4 (NADPH oxidase 4) expression.

174 reactive oxygen species (ROS)-forming Nox5 (NADPH oxidase 5).

175 h production of Igs, or by the activation of NADPH oxidase (NOX) complexes.

176 neutrophils by the electrogenic activity of NADPH oxidase.

177 tuberculosis PPE2 disrupted the assembly of NADPH oxidase complex.

178 nitrite-NO pathway results in attenuation of NADPH oxidase-derived oxidative stress and stimulation o

179 the sufficient intracellular availability of NADPH in strawberry fruits treated with 150 nM PSKalpha.

180 etic reactions, probably as a consequence of NADPH formation in autotrophic organs.

181 The deletion of NADPH oxidase nox1 and its regulator, nor1 in T. guizhou

182 The disruption of NADPH synthesis, due to the non-functional PSI, probably

183 priming phenotypes, including enhancement of NADPH oxidase activity, shedding of l-selectin, or mobil

184 he gut, and twofold higher gut expression of NADPH oxidase (NOX2) and translocator protein (TSPO).

185 Gene expression of NADPH oxidase 2-mediated oxidative stress markers was in

186 ion links diastolic stretch to generation of NADPH oxidase 2 (NOX2)-dependent reactive oxygen species

187 tioxidant capacity through the generation of NADPH; however, its function in non-small cell lung canc

188 te scavenging of superoxide or inhibition of NADPH oxidase improved NO-dependent dilation in MDD.

189 The inhibition of NADPH oxidase-mediated ROS production by pathogen infect

190 uced the progression of EP and the levels of NADPH oxidase.

191 a microtubule-dependent mechanoactivation of NADPH oxidase 2 (NOX2)-generated reactive oxygen species

192 SNO-CoA reductase, as a primary mediator of NADPH-coupled GSNOR activity in these tissues.

193 s and through the differential modulation of NADPH oxidase activity, or the superoxide burst.

194 ica exudates was coupled to the oxidation of NADPH.

195 ggested was mediated via their production of NADPH oxidase-derived reactive oxygen species and MMP-9.

196 racellular Ca2+ signaling and a reduction of NADPH oxidase 2 (NOX2)/ROS production.

197 Growing evidence supports a central role of NADPH oxidases (NOXs) in the regulation of platelets, wh

198 on of cGMP, which prompts the stimulation of NADPH oxidase and protein kinase C (PKC).

199 , the gene encoding the catalytic subunit of NADPH oxidase gp91phox.

200 NA associated with p47phox, a key subunit of NADPH oxidase, and that this association regulated ROS p

201 PE2 interacted with the cytosolic subunit of NADPH oxidase, p67(phox), and prevented translocation of

202 presumably due to the inefficient supply of NADPH, the preferred cofactor of GalA reductases.

203 n was derived from its strong suppression of NADPH oxidase, a key producer of ROS in cells.

204 es neutrophil LTB4 generation as a target of NADPH oxidase regulation, which could potentially be exp

205 system, termed NTRC, which allows the use of NADPH in the redox network of these organelles.

206 aused oxidative stress via direct binding on NADPH oxidase (NOX)4 promoter and induction of NOX4 (NAD

207 formation of the complex could shed light on NADPH oxidase regulation and help identify inhibition si

208 of enzymes such as myeloperoxidase (MPO) or NADPH oxidase, and the release of neutrophil extracellul

209 lectron transport chain composed of NADH (or NADPH), cytochrome b(5) reductase (b(5)R), and cytochrom

210 ld be the lack of reduction factors (NADH or NADPH).

211 reduction of GSNO can involve either NADH or NADPH.

212 de adenine dinucleotide phosphatase oxidase (NADPH oxidase) levels, in comparison to DM+INS and DM+RS

213 1000 fold in the presence of cytochrome P450 NADPH:oxidoreductase (CPR) from the liver and bone marro

214 , focusing on the central role of particular NADPH oxidase (NOX) isoforms that are activated in speci

215 Phagocyte NADPH oxidase but not myeloperoxidase was required for M

216 oduction was dependent on the NOX2 phagocyte NADPH oxidase.

217 These results indicate that phagocyte NADPH oxidase-mediated GAS killing is compromised in the

218 p91phox-p22phox heterodimer of the phagocyte NADPH oxidase in human cells and that EROS mutations are

219 The phagocyte NADPH oxidase is responsible for the neutrophil's great

220 Superoxide anion production by the phagocyte NADPH oxidase plays a crucial role in host defenses and

221 nicotinamide adenine dinucleotide phosphate (NADPH) and NADP(+) are cycled rapidly between ferredoxin

222 nicotinamide adenine dinucleotide phosphate (NADPH) cofactor bound to the oxidoreductase domain(8,9)

223 nicotinamide adenine dinucleotide phosphate (NADPH) is required to mitigate oxidative stress in respo

224 nicotinamide adenine dinucleotide phosphate (NADPH) production, lipogenesis, and colorectal cancers i

225 nicotinamide adenine dinucleotide phosphate (NADPH), and nicotinamide adenine dinucleotide (NADH).

226 tate through the recycling of photosynthetic NADPH.

227 The plant NADPH oxidase RBOHD is a primary player in ROS productio

228 elope of SpNOX, the Streptococcus pneumoniae NADPH oxidase (NOX), a prokaryotic model system for expl

229 Targeted mutagenesis of predicted NADPH- and FAD-cofactor sites resulted in Bs3 derivative

230 ies indicate that this activity is primarily NADPH-dependent.

231 osphorylation, but dependent on ME1-produced NADPH and glutathione (GSH).

232 osphate (NADP(+)) is essential for producing NADPH, the primary cofactor for reductive metabolism.

233 ormazan, (5) S-nitrosothiols did not promote NADPH-dependent reduction of tetra-nitro-blue tetrazoliu

234 rosated proteins such as NOS), which promote NADPH-dependent reduction of NBT to diformazan.

235 that the catalytic activity of NOS promotes NADPH-dependent reduction of nitro-blue tetrazolium (NBT

236 bound enzymes that rely on the same protein, NADPH-cytochrome P450 reductase (POR), to provide the el

237 mulations of the ternary protochlorophyllide-NADPH-POR complex identify multiple interactions in the

238 on of the co-substrate sorbitol in providing NADPH.

239 Here, we de novo purified NADPH-coupled GSNOR activity from mammalian tissues and

240 A putative NADPH-oxidizing flavoenzyme with predicted transmembrane

241 of angiotensin II type 1 receptor (AT(1) R), NADPH oxidase (NOX) subunits, D(5) R, and NaCl cotranspo

242 by acetylcholine in aortic rings and reduced NADPH oxidase activity in DOCA-salt animals.

243 osition of S-nitrosothiols, markedly reduced NADPH diaphorase staining in tissue sections subsequentl

244 JQ1 treatment reduces NADPH subunit transcript levels in mdx muscles, isolated

245 e-phosphate pathway (PPP), which regenerates NADPH to preserve the glutathione redox status and survi

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

247 ytosolic concentration of Ca(2+) and release NADPH oxidase-derived reactive oxygen species.

248 SNO-CoA reductases require NADPH, whereas enzymatic reduction of GSNO can involve e

249 As a result, NADPH-which would otherwise be required for lysine biosy

250 Cell viability, ROS, NADPH, NADH, and ATP levels were fully rescued by TRPM2

251 In this setting, NADPH oxidase, a source of free radicals, decreased in t

252 neuronal intrinsic signaling axis PKC-STAT3-NADPH oxidase 2 (NOX2), enhancing redox signaling as sho

253 at model of HIV, we found increased striatal NADPH oxidase-4 and neuronal nitric oxide synthase expre

254 of MtmW and its complexes with co-substrate NADPH and PEG, suggest a catalytic mechanism of MtmW.

255 ex, in the absence and presence of substrate NADPH, as well as DUOX1-DUOXA1 in an unexpected dimer-of

256 rial pacing model of AF, we demonstrate that NADPH oxidase 2 (NOX2) generated oxidative injury causes

257 We also found that NADPH oxidase (NOX)-mediated oxidative stress occurs at

258 We found that NADPH oxidase 5 (NOX5), mPGES-1 and iNOS were significan

259 Rapid-reaction kinetic analyses showed that NADPH binds tightly (K(D) of ~2 mum) to AsFMO and that t

260 Our results suggest that NADPH diaphorase in aldehyde-fixed tissues is not enzyma

261 The NADPH oxidase complex (NOX) produces reactive oxygen spe

262 by the competitive antagonist AMG-21629, the NADPH oxidase assembly inhibitor apocynin, and the react

263 because multiple oxidoreductases affect the NADPH pool simultaneously.

264 lso suggests that vitamin K1 overlaps at the NADPH binding site of ALR2, which probably shows that vi

265 capacity to generate reactive oxygen by the NADPH oxidase 2 holoenzyme, an enzyme complex highly exp

266 dG and gammaH2AX-which was suppressed by the NADPH oxidase inhibitor diphenylene iodonium and a DUOX2

267 eactive oxygen species (ROS) produced by the NADPH oxidase Nox in enterocytes, are required for p38 a

268 operoxidase uses superoxide generated by the NADPH oxidase to oxidize chloride to the potent bacteric

269 h the former reaction being catalyzed by the NADPH-dependent dehydrogenase CofA.

270 growth and development are controlled by the NADPH/NADPH thioredoxin reductase (NTR)/thioredoxin (TRX

271 ee enzymes (STEAP2-STEAP4) that catalyze the NADPH-dependent reduction of iron(III).

272 idA is an N-monooxygenase that catalyzes the NADPH-dependent hydroxylation of l-ornithine through a m

273 , the overall phenomenon roughly doubles the NADPH demand of the cell.

274 We also report a novel role for the NADPH oxidase enzymes (NOXs), namely NOX1, and NOX-deriv

275 (ROS) derived from mitochondria and from the NADPH oxidase (NOX) enzymes of innate immune cells are k

276 complemented with lipA ROS derived from the NADPH phagocyte oxidase complex and RNS derived from the

277 poorly understood, and establishing how the NADPH oxidase (NOX2) kills microbes has proven elusive.

278 uently, function-disrupting mutations in the NADPH oxidase lead to chronic granulomatous disease, cha

279 important defense components, including the NADPH oxidase RBOHD, ABC-transporter PEN3, calcium-ATPas

280 phox) gene, which encodes a component of the NADPH oxidase 2 complex that mediates neutrophil oxidati

281 al. define a previously unknown role of the NADPH oxidase catalytic subunit NOX5 in cerebral infarct

282 by Akt3 is due to the phosphorylation of the NADPH oxidase subunit p47(phox), which results in NADPH

283 ation to chromatin regulatory regions of the NADPH oxidase subunits increases in the mdx muscle and J

284 brain damage, mediated by activation of the NADPH oxidase, uncoupling of endothelial and neuronal ni

285 Pkc1 phosphorylates the NADPH oxidase regulator NoxR and, collectively, these si

286 vity by the small molecule AZ67 prevents the NADPH oxidation, redox stress and apoptotic cell death c

287 fibrogenic, and pro-oxidant activity via the NADPH oxidase 4.

288 otein kinase activation and possibly through NADPH depletion and subsequent inhibition of BMI1, an in

289 ributed to elevated oxidative stress through NADPH oxidase in lineage-traced microglia.

290 NADP(+) is reduced back to NADPH by activation of mitochondrial membrane potential-

291 hydrogenase (G6PD) is a major contributor to NADPH production and redox homeostasis and its expressio

292 duction pathway linking diastolic stretch to NADPH oxidase 2-derived reactive oxygen species signals

293 eto-l-gulonic acid to l-idonic acid and uses NADPH as preferred coenzyme.

294 The enzyme uses NADPH-cytochrome P450 reductase as a donor of electrons

295 d SORD reduce erythrose to erythritol, using NADPH as a co-factor, and cell culture studies indicate

296 cess, peroxidases play a crucial role, using NADPH provided mostly by nicotinamide nucleotide transhy

297 n of TLR4, MD2, and subunits of the vascular NADPH oxidases under diabetes and hypertension.

298 mon in Asian populations, is not active when NADPH is used as a co-factor in vitro We also confirmed

299 yzes the reduction step of the CB cycle with NADPH to produce the sugar glyceraldehyde 3-phosphate (G

300 We found that allyl mercaptan with NADPH was the preferred substrate-cofactor combination.