ライフサイエンスコーパス: NAD(P)H oxidase

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

2 oduction was dependent on the NOX2 phagocyte NADPH oxidase.

3 ively regulates the abundance of a conserved NADPH oxidase.

4 cular endothelial cell protein expression of NADPH oxidase.

5 a strategy to inhibit assembly of neutrophil NADPH oxidase.

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

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

8 oxygen species generation by neutrophil NOX2 NADPH oxidase.

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

10 neutrophils by the electrogenic activity of NADPH oxidase.

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

12 ROS originate from mitochondria and NADPH oxidases.

13 jor reactive oxygen species-producing enzyme NAD(P)H oxidase.

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

15 another component of the catalytic center of NAD(P)H oxidase.

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

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

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

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

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

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

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

23 1 knockdown resulted in high Rac1 and Nox 1 (NADPH oxidase 1) activity, increased ROS (oxidative stre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 cium homeostasis and heart rhythm by a NOX2 (NADPH oxidase 2)-dependent mechanism.

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

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

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

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

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

47 h factor beta1 (TGFbeta1), endothelin-1, and NAD(P)H oxidase 4 also occur in parallel with Elmo1, as

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 learly identify PAT1 as a novel regulator of NADPH oxidase activation and superoxide anion production

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

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

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

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

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

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

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

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

82 ous heme reversed these effects and restored NAD(P)H oxidase activity.

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

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

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

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

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

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

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

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

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

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

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

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

95 confirming that the current originates from NADPH oxidase activity.

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

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

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

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

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

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

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

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

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

105 Inhibition of NADPH oxidase and myeloperoxidase lowered GSA formation

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

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

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

109 Chemokine-controlled NADPH oxidases and metabolically controlled mitochondria

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

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

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

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

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

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

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

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

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

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

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

121 An NADPH oxidase assay proved that the inhibitory effect of

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

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

124 Phagocyte NADPH oxidase but not myeloperoxidase was required for M

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

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

127 The NADPH oxidase can be assembled in the plasma membrane, a

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

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

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

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

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

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

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

135 tuberculosis PPE2 disrupted the assembly of NADPH oxidase complex.

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

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

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

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

140 NADPH oxidases contribute to LPS-induced reactive oxygen

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

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

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

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

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

146 1 GAS can be cleared by neutrophils using an NADPH oxidase-dependent mechanism in the lung.

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

148 NADPH oxidase-derived excessive production of reactive o

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

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

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

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

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

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

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

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

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

158 .92-7.38] mg/L; P<0.01) and endothelial cell NADPH oxidase expression (P<0.05).

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

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

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

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

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

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

165 Activated NADPH oxidase generates reactive oxygen species and elev

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

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

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

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

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

171 structurally and quantitatively characterize NADPH oxidase in live cells.

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

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

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

175 NADPH oxidase inhibition did not prevent cross-talk inhi

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

177 2X7R agonist, BzATP, and was attenuated by a NADPH oxidase inhibitor apocynin.

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

179 In addition, NADPH oxidase inhibitor diphenylene iodonium significant

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

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

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

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

184 The phagocyte NADPH oxidase is composed of cytosolic components (p40ph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 ines pMF; (2) protein kinase A (PKA) and (3) NADPH oxidase mediate inhibitory interactions between Q

200 generates an anoxic niche to evade phagocyte NADPH oxidase-mediated clearance.

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

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

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

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

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

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

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

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

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

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

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

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

213 nt signaling and epigenetic silencing of the NADPH oxidase (NOX) enzyme DUOX1, both potentially contr

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

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

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

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

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

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

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

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

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

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

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

225 ndent upon reactive oxygen species (ROS) and NADPH oxidase (NOX), both of which are also upregulated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 NADPH oxidase pathway modulators decreased ROS productio

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

256 loroplasts and mitochondria, plasma membrane NADPH oxidases, peroxisomal oxidases, type III peroxidas

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

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

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

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

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

262 Phagocyte NADPH oxidase produces superoxide anions, a precursor of

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

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

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

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

267 1, followed by direct phosphorylation of the NADPH oxidase RBOHD, resulting in elevated production of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

300 ion in oxidative stress by downregulation of NADPH oxidases with no changes in fibrosis.