ライフサイエンスコーパス: NADPH 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 ge was absent in mice that lacked epithelial NADPH oxidase 1 (NOX1) activity.

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

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

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

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

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

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

20 1 knockdown resulted in high Rac1 and Nox 1 (NADPH oxidase 1) activity, increased ROS (oxidative stre

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

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

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

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

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

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

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

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

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

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

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

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

33 y inhibiting Akt kinase activities, reducing NADPH oxidase 2 activation, and lowering phagolysosomal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 confirming that the current originates from NADPH oxidase activity.

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

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

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

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

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

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

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

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

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

99 Inhibition of NADPH oxidase and myeloperoxidase lowered GSA formation

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

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

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

103 Chemokine-controlled NADPH oxidases and metabolically controlled mitochondria

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

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

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

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

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

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

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

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

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

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

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

115 An NADPH oxidase assay proved that the inhibitory effect of

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

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

118 Phagocyte NADPH oxidase but not myeloperoxidase was required for M

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

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

121 The NADPH oxidase, by generating reactive oxygen species, is

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

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

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

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

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

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

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

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

130 tuberculosis PPE2 disrupted the assembly of NADPH oxidase complex.

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

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

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

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

135 NADPH oxidases contribute to LPS-induced reactive oxygen

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

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

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

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

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

141 1 GAS can be cleared by neutrophils using an NADPH oxidase-dependent mechanism in the lung.

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

143 NADPH oxidase-derived excessive production of reactive o

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

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

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

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

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

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

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

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

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

153 .92-7.38] mg/L; P<0.01) and endothelial cell NADPH oxidase expression (P<0.05).

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

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

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

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

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

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

160 Activated NADPH oxidase generates reactive oxygen species and elev

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

162 ymorphism, C242T of the p22(phox) subunit of NADPH oxidase, has been reported to be negatively associ

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

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

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

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

167 structurally and quantitatively characterize NADPH oxidase in live cells.

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

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

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

171 NADPH oxidase inhibition did not prevent cross-talk inhi

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

173 2X7R agonist, BzATP, and was attenuated by a NADPH oxidase inhibitor apocynin.

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

175 In addition, NADPH oxidase inhibitor diphenylene iodonium significant

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

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

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

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

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

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

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

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

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

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

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

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

188 lucose-induced matrix expression through the NADPH oxidase isoform, NOX4.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 oving electrical charge across the membrane: NADPH oxidase moves electrons and HV 1 moves protons.

206 im of this study was to evaluate the role of NADPH oxidase (NADPHox) in the pathogenesis of oxidative

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 NADPH oxidase pathway modulators decreased ROS productio

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

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

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

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

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

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

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

261 Phagocyte NADPH oxidase produces superoxide anions, a precursor of

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

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

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

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

266 1, followed by direct phosphorylation of the NADPH oxidase RBOHD, resulting in elevated production of

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

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

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

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

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

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

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

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

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

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

277 ages on heart rapidly through a ROS-p38 MAPK-NADPH oxidase-ROS positive feedback loop in response to

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.